This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Neddylation is the process by which the molecule NEDD8 is attached to cellular proteins. Elevated neddylation in the body has been linked to various cancers. Inhibiting this protein modification has therefore become a promising anticancer strategy. A new study describes how researchers used this anti-neddylation approach to kill esophageal cancer cells. The team treated lab-grown esophageal cancer cells with MLN4924, a known neddylation inhibitor. They found that MLN4924 indirectly led to the programmed cell death, or apoptosis, of the cancer cells. By reducing neddylation, MLN4924 actually promoted a cell survival mechanism known as autophagy. Autophagy keeps cells healthy and alive by clearing harmful debris. Interestingly, it also gave the researchers access to a “kill switch” for diverting from autophagy to apoptosis. That switch came in the form of the protein ATF3, which can be silenced to cause cell death..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Acute lymphoblastic leukemia (ALL) is the most common cancer in children, and 85% of cases are B-cell ALL (B-ALL). Although the prognosis is usually good, 10–15% of patients have relapsing or refractory disease, which can lead to poor outcomes. To aid in the development of better treatments for these patients, a new study investigated the role of netrin-1 in B-ALL, as this axon guidance protein has been linked to tumorigenesis in many cancers. In the study, serum netrin-1 levels were higher in children with B-ALL than in children without cancer, and when the children with B-ALL were grouped by risk stratification, the high- and intermediate-risk groups had higher netrin-1 levels than the low-risk group. In vitro, recombinant netrin-1 prevented apoptosis of B-ALL cells, thus supporting cancer cell survival by interacting with the receptor Unc5b to activate the FAK-MAPK pathway. However, netrin-1 did not affect B-ALL cell migration..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Combination therapy with BRAF and MEK inhibitors have become the standard of care for patients with metastatic melanoma harboring BRAF mutations. But one persistent problem is the emergence of drug resistance. A new study reports that one way to overcome this obstacle could be the incorporation of reverse transcriptase inhibitors, or RTIs. RTIs target genetic elements called retrotransposons, which are activated by tumor formation and have been frequently used in treating HIV. Combining the RTI SPV122 with BRAF and MEK inhibitors was shown to have a favorable effect against BRAF-mutant melanoma, inhibiting cell growth, inducing cell death through apoptosis, and delaying the emergence of drug resistance. Further experiments revealed the RTI mechanisms giving rise to these effects, including DNA double-strand breaks, mitochondrial membrane depolarization and increased levels of reactive oxygen species..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Glioma is the most common primary brain tumor and represents a major health problem across the globe. Understanding how gliomas form has proven difficult, especially at the molecular level, but growing evidence points to the important roles played by non-coding RNAs, especially small non-coding RNAs that interact with PIWI proteins, or piRNAs. piRNAs execute functions associated with epigenetic reprogramming and can regulate transcription, translation, development, and mRNA stability. In fact, piRNAs have been detected in many types of cancer and are known to be involved in the development and spread of certain tumors. piRNAs are formed either through the “primary processing pathway” or the secondary “ping-pong cycle” pathway. In conjunction with PIWI proteins, piRNAs execute epigenetic regulation of genes by modifying histones. In this way, piRNAs can influence numerous molecular signaling pathways associated with the formation and spread of gliomas, including the PI3K/AKT and TNF signaling pathways..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"The protein IFNα can reduce growth and promote apoptosis of cancer cells by stimulating genes such as PML, whose deficiency is linked to tumorigenesis, but the contributions of different PML isoforms to the anticancer effects remain unclear. Given that PML-II positively regulates genes that are induced during the type I IFN response, researchers recently investigated whether and how PML-II participates in IFNα-induced cell death using a cervical cancer cell line. In cells with PML-II deletion (siPML-II), death during IFNα stimulation was reduced, and IFNα-induced ISG54 mRNA expression was attenuated. In addition, silencing PML-II decreased the expression of TRAIL and PUMA during IFNα stimulation, indicating that the extrinsic and intrinsic apoptosis pathways were blunted..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Cancer remains the second leading cause of death worldwide, partly because cancer cells can resist chemotherapy. In one resistance mechanism, the Nrf2 signaling pathway helps cancer cells survive the oxidative stress induced by chemotherapy drugs. Therefore, compounds that inhibit Nrf2, like phenolic compounds, might be promising anticancer agents. Phenolic compounds are abundant in traditional herbal products known for their anticancer effects, such as ginger, turmeric, and green tea. Some phenolic compounds, like those in Chinese cinnamon, keep Nrf2 from entering the nucleus, where it normally exerts its activity, while others, like those in yellow azalea, prevent Nrf2 expression. These changes in turn block Nrf2-mediated antioxidant systems, making the cancer cells susceptible to drug-induced oxidative stress or even inducing cell death without the help of other cancer-fighting drugs..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Phospholipid scramblase 1 (PLSCR1) is the most studied member of its protein family and has a complex array of suggested functions. While PLSCR1 was first described as a plasma membrane protein, it has subsequently been found in other cellular compartments and implicated in numerous cellular pathways including apoptosis, intracellular trafficking of membrane proteins, and pro-inflammatory events. PLSCR1 interacts with various effectors, mediators, and regulators that then contribute to distinct cellular processes. While most PLSCR1 interactors are thought to be cell-type specific, the mechanisms of PLSCR1's regulatory functions are often shared. But not all PLSCR1 interactors are endogenous in origin; PLSCR1 also interacts with exogenous viral proteins. These interactions regulate viral uptake and spread in both pro- and anti-viral ways..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Familial adenomatous polyposis (FAP) is an inherited disorder characterized by the formation of up to several thousand tumors in the rectum and colon. FAP is usually caused by a mutation of the adenomatous polyposis coli (APC) gene. While the molecular changes linking this mutation to tumor formation are not fully understood, dysregulated apoptosis—a form of programmed cell death—is known to play a prominent role. Now, researchers have uncovered a pattern of expression of an apoptosis-regulating protein that may help explain how FAP tumors form. The protein is called apoptosis repressor with caspase recruitment domain, or ARC. The team examined the expression of ARC in 212 FAP tumor samples from 80 patients. They found that ARC was expressed in the cytoplasm of most tumor cells, as well as in the nuclei..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"The human protein Tid-1 sits at the nexus of many key cellular processes and signaling pathways. These processes include cellular proliferation, growth, survival, aging, apoptosis, and even movement. Tid-1 is a member of the heat shock protein 40 family and helps other proteins fold correctly after translation or refold after a damaging stress event. Dysregulated Tid-1 behavior is involved in numerous human diseases including cancers, cardiomyopathies, and neurodegenerative disorders. Given its wide influence within the cell, Tid-1 could be a key biomarker or even therapeutic target for these diseases, but to leverage Tid-1 effectively, researchers need to understand its functionality in detail. To this end, a team of scientists consolidated the current research on human Tid-1. They found that Tid-1’s protein-protein interactions corresponded to its roles in various diseases and provide insight into how Tid-1 affects pathogenic developments..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"All that lives will die. Our cells are the building blocks of life, and regulated, or programmed, cell death is a critical ubiquitous process. Without it our tissues would be unable to stay balanced. In spontaneous cell death, necrosis, the cell suddenly ruptures and damages those around it. However, the disruption of regulated cell death plays key roles in many human diseases. Particularly neurodegenerative diseases, which often include widespread death of neurons. A recent review paper highlights five major types of regulated cell death. The first type, apoptosis, is classic programmed cell death, which is organized and largely immune silent. Then pyroptosis, a highly inflammatory form of cell death where the cell membrane ruptures. Autophagy-dependent cell death ramps up the cellular process autophagy, which recycles cellular components into usable metabolites. Necroptosis is a very necrosis-like type of cell death, but unlike true necrosis it is regulated rather than spontaneous..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Our bodies must undergo tissue self-renewal in order to remain healthy, and cell death is an important part of self-renewal. Apoptosis is a mechanism of programmed cell death that maintains homeostasis without inflammation. As dying cells begin to dismantle, they signal to phagocytes to engulf them, a process called efferocytosis. The balance between these “find-me,” “eat-me,” and “don’t-eat-me” signals is critical. Unfortunately, because efferocytosis prevents inflammatory responses, these signaling pathways are often hijacked by cancer cells to facilitate immune escape. Although traditional cancer therapies, such as chemotherapy and radiation, kill cancer cells directly, the resulting apoptosis can increase efferocytosis and suppress the immune response, allowing for progression of residual cancer. A new strategy is to combine traditional therapies with those that inhibit efferocytosis, killing tumor cells while blocking the pathways that allow them to proliferate..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Breast cancer accounts for more than 6% of all cancer-related deaths worldwide; the main cause of death being metastasis to other tissues. One factor that leads to this spread is breast cancer’s resistance to chemotherapy. A recent study reveals a molecular target that could curb the persistent progression of breast cancer. The protein RelB was observed to be overexpressed in human breast cancer tissue promoting cancer cell proliferation by decreasing normally programmed cell death and increasing cell mobility. Genetically switching RelB expression off dramatically reduced and even prevented breast tumor growth in mice. RelB’s cancer-promoting functions are linked to its activation of the noncanonical NF-κB signaling pathway, which helps sustain breast cancer metastasis under low-estrogen conditions. Targeting this under-examined pathway could be one way to prevent the spread of breast cancer cells and thereby boost anti-cancer therapies for millions of patients around the globe..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Bladder cancer is the 10th most frequent malignancy in the world. Despite the availability of several treatment options, including surgery, chemotherapy, and radiotherapy, outcomes for patients with bladder cancer remain poor. Fortunately, a growing understanding of the molecular origins of the disease is revealing new targets for treatment. Among the most promising are a family of enzymes called tyrosine kinases. Tyrosine kinases modify the structure and function of tyrosine-containing proteins. This action helps regulate cellular processes such as growth, migration, differentiation, and metabolism. Dysregulation of tyrosine kinases is part of the pathway that leads to signs and symptoms of bladder cancer. Abnormal tyrosine kinase function can be caused by mutations, amplification, and chromosomal abnormalities. Ongoing studies are discovering how tyrosine kinases can serve as early markers of bladder cancer and how they might be manipulated to stop the progression of bladder tumors..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Phosphatidylserine (PS) is a fatty substance normally located on the inner membrane of healthy cells, but cancer cells tend to express high levels of PS on their surface. That tiny difference has paved the way for a new cancer-targeting agent called SapC-DOPS. SapC-DOPS is a nanovesicle that effectively targets and kills several types of cancer, including pancreatic, lung, brain, and pediatric cancers, while leaving surrounding cells unharmed. The nanovesicle achieves this by selectively inducing apoptotic cell death in malignant and metastatic cancer cells rich in surface PS. One phase I clinical trial showed that SapC-DOPS was safe and yielded favorable outcomes in patients with solid tumors, but more pre-clinical studies are needed to better understand the properties of SapC-DOPS, including how SapC-DOPS can eliminate cancer cells that express high levels of surface PS but evade apoptotic cell death and how effective SapC-DOPS is in treating advanced cancers..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Temozolomide , or TMZ , is a chemotherapy agent used to treat glioblastoma. TMZ causes DNA damage that results in tumor cell apoptosis and thereby increases the survival rate of patients with glioblastoma. Over time, however, glioblastoma cells can become less responsive to TMZ because the drug induces autophagy in these cells, clearing otherwise toxic cargo and saving the cells from premature death. This chemoresistance can prove fatal for patients who rely on the anti-cancer effects of TMZ. Now, researchers have discovered a way to keep TMZ working long-term: by combining it with the cholesterol-reducing statin simvastatin , or Simva. Previous studies have shown that long-term consumption of statins prior to or in addition to cancer therapeutics can increase the survival rates of patients with different forms of cancer. Simva is shown to be less toxic towards the liver and gastrointestinal tract than other statins and can cross the blood-brain barrier to target glioblastoma cells..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Chronic myeloid leukemia (CML) is a rare, spontaneous cancer found in bone marrow. Often the causative mutation generates a fusion protein, BCR-ABL1, with abnormal tyrosine kinase activity, and that abnormal activity is the target of the current tyrosine kinase inhibitor treatments. However, these treatments are expensive if used long term and do not kill cancerous stem cells. Thus, new treatments and treatment targets are needed. One potential category of targets are transcription regulators, such as CDK9 (cyclin-dependent kinase 9). Wogonin is a naturally occurring inhibitor of CDK9, and in a recent study it showed anti-CML effects on cell lines and primary CML cells. Specifically, wogonin induced erythroid differentiation in CML cell lines and primary cells and apoptosis in the KU-812 cell line. Wogonin treatment increased binding between GATA-1 and FOG-1, key players in erythrocyte differentiation and decreased binding between GATA-1 and RUNX1, which regulate megakaryocyte differentiation..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Phosphatidylserine (PS) is a lipid found in the cell membrane. When exposed on the outside of a cell during stress or during cell death, PS can trigger immune suppression. PS also engages PS receptors on immune cells, resulting in clearance of the cell and production of immune suppressive factors. One way tumors evade the host immune system is by engaging PS signaling. Therefore, inhibiting PS signaling suppression is a promising option for treating cancer. A recent review highlights the contributions of the TIM and TAM family of receptors to PS signaling and immune suppression in tumors. and some of the immunotherapy strategies targeting these receptors that are being investigated in preclinical and clinical trials. Due to the complexity of PS-induced immune suppression, there are still many unknowns. such as the detailed mechanisms and signaling pathways that are involved. or the consequences of interrupting these signaling pathways..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Targeted therapy with BRAF and MEK inhibitors has significantly improved the outcomes of patients with BRAF-mutated metastatic melanoma. Unfortunately, a combination of genetic and epigenetic events can create resistance to such treatment, causing most patients to relapse. A new study suggests that this resistance could be due to dysregulation of the miR-146a-5p-regulated NFκB signaling network. Initial experiments showed the gene COX2 to be largely regulated by miR-146a-5p and NFκB. Further experiments involved manipulating miR-146a-5p/COX2 in vitro and in 3D cultures of treatment-resistant tumors explanted from patients undergoing therapy, which demonstrated that miR-146a-5p expression increased drug sensitivity and reduced COX2 expression. Tumor cells’ susceptibility to therapy could be significantly enhanced by decreasing COX2 expression through forced miR-146a-5p expression or by inhibiting COX2 expression with the drug celecoxib..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Cholangiocarcinoma (CCA) is an aggressive form of cancer that forms in the biliary tract. CCA has high mortality and high rates of recurrence. While early diagnosis is critical, the molecular mechanisms by which CCA forms are poorly understood. A new study reports key interactions between three proteins during CCA development: TLR3, a mediator of both innate and adaptive immune responses and a promising target for anti-cancer therapy; IAP proteins that regulate apoptosis and orchestrate cancer cell death; and RIPK1, a multifunctional protein that regulates inflammation and cell death through apoptosis and necroptosis.TLR3 expression was found to be significantly higher in primary CCA tissue than in adjacent normal tissue. Meanwhile, Smac mimetic, an IAPs antagonist, sensitized CCA cell lines to TLR3 ligand, Poly(I:C)-induced apoptosis. This mode of cell death was switched to necroptosis in CCA cells expressing RIPK1, RIPK3, and MLKL..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Phosphorylated STAT1 (P-STAT1) is an important mediator of interferon-induced antiviral immunity. During interferon signaling, P-STAT1 dimerizes and accumulates in the nucleus with the help of the protein importin to affect gene transcription and elicit immune responses. In a positive feedback loop, P-STAT1 also induces further STAT1 expression, thereby increasing the cytoplasmic levels of unphosphorylated STAT1 (U-STAT1), a protein that regulates apoptotic cell death. However, the impact of U-STAT1 on the P-STAT1-mediated immune response is unclear. To learn more, researchers recently cotransfected cells with wild-type P-STAT1 and a permanently unphosphorylated U-STAT1 mimic. Interestingly, the U-STAT1 mimic prevented nuclear accumulation of P-STAT1 during interferon gamma (IFNγ) stimulation, but it didn’t impair downstream P-STAT1 signaling, indicating that some P-STAT1 could still enter the nucleus to exert its effects..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.