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 remains one of the most common cancers among women, indicating that better treatments are needed. The drug THZ1 is effective against triple-negative breast cancer, which frequently features overexpression-inducing mutations in the protein p53. However, THZ1 is ineffective against breast cancer cells with nonmutated (wild-type, WT) p53. To improve treatment options, researchers recently tried to increase the THZ1 sensitivity of WT p53 breast cancer cells. Treating the cells with nutlin-3, a molecule that indirectly prevents p53 degradation, enhanced the killing ability of THZ1, and overexpression experiments confirmed that this sensitization was due to upregulation of functional p53. Further investigation into the mechanism revealed that p53 accumulated in the nuclei and mitochondria of the dying cells after nutlin-3 and THZ1 treatment..."

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:

"Pancreatic neuroendocrine tumors, or PNETs, are a form of cancer that invade the hormone-producing cells in the pancreas. While many are benign, PNETs tend to behave unpredictably. And many treatments against malignant PNETs have proven ineffective. Now, a new study suggests that the anti-inflammatory herbal blend Zyflamend could be a promising treatment option. Experiments showed that Zyflamend reduces cell survival and induces cell death in pancreatic cancer cells in a dose-dependent manner. Zyflamend does so by inducing apoptosis, a programmed death sequence initiated by discarded cells. This form of cell death appears to be mediated by the JNK pathway, an important part of inflammatory responses in mammals. Although more work is needed to understand the full effects of this herbal blend in the clinic. These findings suggest that Zyflamend could be a novel add-on therapy for treating pancreatic 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:

"Lung cancer remains a major cause of cancer-related death worldwide, indicating that better treatments are needed. One way to develop new treatments while saving time and money (and reducing the risk of unexpected side effects) is by repurposing drugs that are currently used for other diseases. For example, ciclopirox olamine (CPX) is an iron-binding antifungal agent that has been found to be effective against a variety of cancers. Researchers recently investigated the efficacy of CPX against non-small-cell lung cancer (NSCLC). In vitro, CPX inhibited cell proliferation, migration, and invasion in two NSCLC cell lines. Specifically, it blocked the epithelial–mesenchymal transition, a shift that allows cells to become mobile. CPX also disrupted cellular energy processes and promoted toxic reactive oxygen species production, leading to buildup of improperly folded proteins in the endoplasmic reticulum and ultimately causing cell death via apoptosis..."

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:

"Diabetic retinopathy (DR) is a severe ocular complication of diabetes mellitus, affecting over 400 million adults worldwide and causing blindness in millions of them. Neurodegeneration is an early event in DR pathogenesis, preceding clinically detectable vascular damage. One potential cause of neuronal loss in DR is the dysregulated autophagy. Unfortunately, the mechanisms underlying autophagy dysregulation in DR remain unclear. A new study focused on the role of a central signaling molecule in this process, mTOR (mechanistic target of rapamycin) is a ubiquitous molecule that integrates diverse underlying signals to coordinate biological processes. Using a mouse model of DR, researchers found that mTOR-related proteins were upregulated shortly after diabetes induction but were then downregulated. Diabetes-induced neurodegeneration observed in this study was evaluated by an increase of apoptosis markers and a decrease in the total cell number..."

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:

"Polycystic ovary syndrome (PCOS) is a common endocrine disease usually accompanied by infertility. In PCOS, granulosa cells (GCs) produce insufficient energy via glycolysis to support proper follicle (egg-releasing sac) development, resulting in a condition called follicular dysplasia. miRNAs in small vesicles (exosomes) within the follicular fluid can regulate GCs, but whether these miRNAs affect GC glycolysis in PCOS is unclear. To find out, a recent study sequenced the RNA in exosomes from clinical follicular fluid samples. Compared to controls, exosomes from patients with PCOS had higher levels of the miRNA miR-143-3p and lower levels of the miRNA miR-155-5p. Glycolysis pathways were also negatively regulated in PCOS exosomes. In vitro, experiments on a KGN cell PCOS model confirmed that miR-143-3p inhibited glycolysis by silencing the gene HK2. miR-155-5p normally blocks miR-143-3p’s activity, so the miR-155-5p downregulation in PCOS permitted miR-143-3p to silence HK2..."

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:

"Liver cancer is the third deadliest cancer worldwide, and effective treatments are limited. But inducing apoptosis, a type of programmed cell death, could aid or replace current treatments. Apoptin is a protein that triggers apoptosis specifically in tumor cells. Apoptin also activates autophagy, or the breakdown of unneeded or damaged cellular components, which can either inhibit or induce apoptosis. However, the cellular mechanisms linking these processes remain unclear. So, researchers recently used cultured liver cancer cells and a mouse model of liver cancer to elucidate those mechanisms. First, they confirmed that apoptin increased apoptosis and autophagy in both the cultured cells and the mice. But they also found that the autophagy it activated was protective, slowing the rate of apoptosis. Mechanistically, apoptin increased the levels of reactive oxygen species (ROS) and activated mitophagy, a mitochondria- specific type of autophagy..."

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:

"In nerve cells, the waxy molecule ceramide plays roles in both cellular differentiation and death, but a new study shows those roles could vary based on how ceramide is formed. Ceramide is generated via 3 pathways: newly from palmitoyl-CoA and serine, from the breakdown of sphingomyelin, and through the endosomal salvage pathway. Experiments showed that blocking ceramide synthesis did not alter ceramide levels in PC12 cells, which require nerve growth factor (NGF) to survive and differentiate, but blocking synthesis did decrease ceramide levels in TrkA cells, which differentiate spontaneously. Blocking sphingomyelin breakdown, however, inhibited differentiation and reduced ceramide in both cell lines. Without NGF, PC12 cells begin to atrophy and die, and preventing sphingomyelin breakdown did not protect them, but it did suppress rising ceramide levels to some degree versus controls..."

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:

"Retroperitoneal liposarcoma (RPLS) is a type of cancer that begins in fat cells and affects soft tissues deep within the body. Recurrence is common because the tumor size and location make complete surgical removal challenging and other treatment strategies are limited due to an incomplete understanding of the factors driving RPLS progression. To gain insight into this process at the molecular level, researchers set out to uncover the role of the cell ion channel TRPM2-S, which allows calcium and other ions to enter the cell and is often associated with cancer. The team showed that high TRPM2-S expression by RPLS cells was associated with higher patient survival than lower levels of TRPM2-S expression. They also found that TRPM2-S can increase the concentration of reactive oxygen species (ROS) within the cell by inhibiting the transcription factor FOXO3a leading to cell proliferation under normal oxygen concentrations but increased cell death under the stress caused by ROS toxicity..."

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