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:

"These tiny sacs within cells are called multivesicular bodies, or MVBs. Once considered nothing more than a part of the cell’s waste disposal and recycling system, MVBs are now understood to play multiple important roles, including promoting tumor progression. MVBs selectively load substances such as lipids, proteins, and nucleic acids, and then fuse with the cell membrane to release their payloads outside the cell in the form of exosomes. In tumors, the key proteins involved in MVB formation, transport, and fusion are abnormally expressed, and evidence suggests that MVBs promote virtually all aspects of cancer progression – from tumor expansion to drug resistance. For example, MVBs direct the cellular degradation needed for cancer cells to form the finger-like projections that help them spread to other organs, and studies show that MVB cargoes can transfer cancer drug resistance from one cell to another..."

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:

"N6-methyl-adenosine (m⁶A) methylation is the most abundant epigenetic modification on mRNA and lncRNA. This modification is regulated by m⁶A writers, readers, and erasers, and its proper regulation is critical for innate and adaptive immunity, especially since m⁶A can play different roles depending on the transcript region, cell type, or specific regulators involved. For example, in the innate immune system, m⁶A can promote the antitumor and antiviral activity of NK cells. It can also activate disease- fighting M1 macrophages, reduce inflammation, and encourage dendritic cell maturation and activity. On the other hand, m⁶A can prevent dendritic cells from cross-presenting tumor antigens to prime T cells, hindering the antitumor response. In the adaptive immune system, m⁶A promotes T cell homeostasis but also suppresses T follicular helper cell development and it can either exacerbate or inhibit HIV-1 infection in CD4⁺ T 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:

"Transcriptional regulation is an important and complex process whose dysregulation can lead to disease. For example, aberrant activation of signaling involving the transcriptional activator Notch drives many processes in tumor formation. However, the exact mechanism by which Notch regulates transcription remains unclear. To find out more, researchers recently used various protein biochemistry and molecular biology approaches to analyze the composition and functions of the Notch supercomplex. They found that the INT complex is part of the Notch transcriptional supercomplex and works together with NACK to activate Notch-mediated transcription. Specifically, NACK is needed for recruitment of the transcribing enzyme RNAPII to Notch-dependent gene promoters, while the INT complex is needed for phosphorylation of RNAPII at serine 5, which induces transcription..."

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:

"Non-small cell lung cancer (NSCLC) remains deadly, indicating a need for better diagnosis and treatment strategies. The protein OVOL2 is known to suppress tumor development in NSCLC and other cancers. However, it’s unclear whether OVOL2 exerts its anticancer effects by disrupting aerobic glycolysis, the main energy pathway in tumor cells. To find out, researchers recently investigated OVOL2 signaling in NSCLC. OVOL2 was downregulated in NSCLC cells and mouse NSCLC tissues compared to normal lung (NL) samples. Specifically, OVOL2 was negatively regulated by NF-κB signaling via the ubiquitin–proteasome degradation pathway. However, lentivirus (LV)-mediated overexpression of OVOL2 reduced NSCLC cell survival in vitro, and OVOL2 impaired aerobic glycolysis in NSCLC cell lines and mouse xenograft models. OVOL2 exerted its beneficial effects by binding to P65 and inhibiting P300 recruitment while facilitating HDAC1–P65 binding..."

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

Students learn about the biomedical use of nanoparticles in the detection and treatment of cancer, including the use of quantum dots and lasers that heat-activate nanoparticles. They also learn about electrophoresis a laboratory procedure that uses an electric field to move tiny particles through a channel in order to separate them by size. They complete an online virtual mini-lab, with accompanying worksheet, to better understand gel electrophoresis. This prepares them for the associated activity to write draft research proposals to use nanoparticles to protect against, detect or treat skin cancer.

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:

"Pancreatic ductal adenocarcinoma (PDAC) is one of the most common causes of cancer-related death globally and is increasing in incidence. While some cancers can be effectively treated with immune checkpoint blockade (ICB) therapy, no such treatments currently exist for PDAC, and no effective biomarkers of this disease have been identified. Recently, researchers demonstrated the ability to shrink PDAC tumors in mice using the drug silvestrol. PDAC is associated with mutations in the KRAS gene that cause the excessive production of proteins involved in normal cell functioning, such as ARF6, AMAP1, and MYC. Interestingly, while silvestrol tended to promote tumor growth in mice with PDAC when administered alone, when combined with anti-PD-1 therapy, a form of ICB treatment, silvestrol reduced the size of PDAC tumors by disrupting the ARF6-AMAP1 pathway in KRAS-mutated 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:

"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:

"Cold shock domain containing E1, or CSDE1, is emerging as a powerful protein in the cell. Growing evidence suggests that CSDE1 reprograms how RNA codes are ultimately translated into proteins, which means CSDE1 could be pivotal in how cells respond to internal and external changes like those brought on by disease. In a new review, researchers outline a model that could explain CSDE1’s reprogramming ability. According to the model, CSDE1 acts as a connector between RNAs and the specific proteins capable of regulating or altering those RNAs. For regulating proteins that can’t normally bind to RNAs, CSDE1 provides a bridge between the two. For proteins that do bind to RNAs, CSDE1 enhances that connection, and for proteins that can but don’t typically bind to certain RNAs, CSDE1 reshapes those RNAs to make binding possible. How CSDE1 connects proteins to RNAs in response to stress isn’t yet clear, but equipped with this new model, researchers could begin to understand CSDE1’s role in human disease..."

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:

"Sialic acids are a family of sugars found throughout the body. They facilitate a variety of cellular functions such as interactions between cells and the detection of foreign bodies. But sialic acids are also linked to the progression of cancer, including bladder cancer. In a new study, researchers examined how bladder cancer cells rich in sialic acids respond to NEU1, one of several enzymes responsible for removing sialic acids from lipids and proteins. The team found that low NEU1 expression was linked to abnormally large amounts of sialic acids in cancer cells. In fact, low expression of NEU1 correlated with bladder cancer progression. High NEU1 expression, on the other hand, enhanced cancer cell death and decreased cancer proliferation. These findings were obtained for both cancer cells grown in the lab and cells extracted from mice with bladder cancer..."

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:

"This is α5-nicotinic acetylcholine receptor (α5-nAChR). Studies have shown that α5-nAChR plays a role in both lung cancer and nicotine dependence. Interestingly, smokers with lung cancer also show higher expression of PD-L1, a separate receptor that cloaks cancer cells from the immune system. To understand whether α5-nAChR and PD-L1 might work together, researchers monitored both receptors in tissue from smokers and nonsmokers with lung cancer and in human tissue implanted into mice. Staining revealed that both α5-nAChR and PD-L1 levels were elevated in lung cancer tissue (carcinoma) versus surrounding tissue (paracarcinoma) and more so in tissue from smokers than in tissue from nonsmokers. Further experiments showed that α5-nAChR could suppress immune cell activity by regulating the expression of PD-L1. In lung cancer tissue grafted into mice, overexpression of α5-nAChR enhanced tumor growth..."

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:

"Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disorder, affecting over 25% of adults worldwide. It causes inflammation and other health conditions, including hepatocellular carcinoma (HCC), a leading cause of cancer-related death. Recently, researchers have looked toward the use of senolytic drugs as a promising treatment. Senolytic drugs selectively target aging cells that no longer divide, which are associated with NAFLD-induced HCC. In a recent study, mice were given low-dose diethylnitrosamine (DEN) and a high-fat diet (HFD) to induce NAFLD-induced HCC. These and normal (CTL) mice were treated with a mixture of two senolytic drugs, dasatinib and quercetin (D+Q). Unexpectedly, the D+Q cocktail had no effect or even worsened liver disease progression in the mice and slightly increased liver damage and tumor generation. The drug cocktail also did not reduce the number of aging cells in the mouse liver, as indicated by the genetic marker p16..."

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 is a devastating disease that progresses when cells divide uncontrollably and spread to other parts of the body, but scientists have found that neighboring noncancerous cells are often able to inhibit the growth of tumor cells in a process known as contact normalization. Tumor cells must somehow overcome this inhibition to become malignant, but exactly how they do this has not yet been resolved. To fill this gap, researchers recently used microscopy, CRISPR, and RNA sequencing techniques to uncover how noncancerous cells influence adjacent cancerous cells. They found that contact normalization takes place when noncancerous cells use the protein N-cadhedrin to adhere to neighboring tumor cells. This results in a decrease in the expression of the protein podoplanin and the inhibition of tumor cell proliferation. The team also concluded that the presence of podoplanin enables cancerous cells to override contact normalization under continued N-cadherin expression..."

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:

"Despite advances in therapy, the prognosis and survival of patients with glioblastoma remain dismal. Part of the reason is poor targeting. The sheer complexity of tumor growth at the molecular scale makes it difficult to pinpoint the origin of gliomas. In recent years, more targeted research has led to the discovery of chains of molecular events that regulate glioma development, including the unusual trafficking of proteins into the nucleus of glioma cells. In a new study, researchers examined this glioma-related behavior for the protein doublecortin (DCX). DCX is a neuronal protein crucial for the formation of new neurons in adulthood and for neuronal migration. While researchers have looked at how glioma cells shuttle different proteins to their nucleus, this marked the first time that scientists zeroed in on DCX. The team found that high accumulation of DCX in the nucleus boosted the invasiveness of glioma cells, whereas blocking the nuclear import of DCX reduced glioma proliferation..."

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:

"Non-small cell lung cancer (NSCLC) is the most common form of lung cancer, and it tends to have a poor prognosis. For NSCLC with EGFR gene mutation, the tyrosine kinase inhibitor osimertinib can be an effective targeted therapy. However, patients usually develop resistance to osimertinib over time, often due to additional changes in the EGFR gene. For example, tumors can develop mutations in exons 18 and 20 of EGFR that reduce osimertinib's ability to bind to its target. In addition, the EGFR gene can become amplified, leading to extra copies in the genome. This leads to abnormally high amounts of the EGFR protein, overwhelming osimertinib and triggering signaling pathways that promote cancer progression. Over time, tumor cells with resistance-promoting mutations can replace the original drug-sensitive cells that are killed off by osimertinib. Combination therapies or next-generation tyrosine kinase inhibitors might help address these limitations of osimertinib..."

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:

"Oncogenic PIM kinases and the tumor suppressor LKB1 regulate cell growth and metabolism in different directions. LKB1 suppresses tumorigenesis largely by phosphorylating and activating the energy sensing kinase AMPK. Anti-oncogenic PIM inhibitors also increase AMPK phosphorylation. However, the exact mechanism by which PIM inhibition affects AMPK remains unclear. A recent study explored the potential PIM-LKB1 interaction related to AMPK phosphorylation in prostate (PC3) and breast (MCF7) cancer cells. Inhibition of activity (by DHPCC9 or AZD1208) or expression (by triple knockout, TKO) of all three PIM kinases increases AMPK phosphorylation. These effects are LKB1-dependent, suggesting that PIM kinases regulate AMPK via LKB1. Additional assays confirmed that PIM kinases phosphorylate LKB1 to inactivate it, identifying LKB1 as a novel PIM substrate. In a chick embryo xenograft model, LKB1 knockout increased tumorigenic growth of prostate cancer 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:

"Prostate cancer is the second-most diagnosed cancer in men worldwide. Development of prostate cancer relies on androgen receptor (AR), a transcription factor that induces the activation or repression of prostate-specific genes. A recent study examined the role of a previously unexplored factor in regulating AR activity. Long intergenic non-coding RNA PVT1 is associated with AR in prostate cancer cells, but its involvement in downregulating gene expression has not been examined. Using a prostate cancer cell line, researchers silenced PVT1 expression. They found that in androgen-stimulated cells, PVT1 knockdown altered the expression of hundreds of genes. A total of 160 genes were upregulated after PVT1 silencing that are typically repressed by AR, including a set of tumor suppressor genes and 121 of the genes affected by PVT1 knockdown were correlated with prostate cancer aggressiveness in the patient cohort..."

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:

"Multiple myeloma (MM) is a common type of plasma cell cancer that remains aggressive and incurable despite the development of several treatments. Approximately 70–80% of patients with MM have myeloma bone disease, which involves bone fractures and high blood calcium (Ca2+) and affects MM prognosis. Various calcium channels and transporters help balance calcium levels, so they may be closely related to MM prognosis. For example, plasma membrane calcium channels allow calcium ions to enter cells, while proteins involved in store-operated calcium entry (SOCE) mediate calcium release from sites in the endoplasmic reticulum (ER)/sarcoplasmic reticulum (SR). Mitochondrial calcium channels regulate calcium uptake into mitochondria, which contributes to SOCE, and calcium-ATPases pump calcium ions from the cytoplasm back into the ER/SR or extracellular space. These molecules have been reported to be altered in the context of MM, but the specific mechanism by which their dysfunction leads to MM remains unclear..."

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 is the most common cancer among women, and some subtypes remain difficult to treat. The tumor microenvironment is known to play a key role in breast cancer progression, but how specific microenvironments affect the secretion of cancer-related proteins remains unclear. To clarify this issue, a new study cultured two breast cancer cell lines, MCF7 and MDA-MB-231, in scaffolds derived from patient breast tumors. Application of culture medium from scaffold-cultured cells to normally cultured cancer cells increased cancer stem cell activity, an important driver of cancer metastasis. Molecular analysis revealed that scaffold-cultured cancer cells secreted more and different proteins than normal monolayer-cultured cells and that culturing cells with scaffolds derived from different patients resulted in different secretion profiles..."

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