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 a leading cause of cancer-related death among women worldwide. One process that fuels the proliferation, survival, and migration of breast cancer cells is aerobic glycolysis. In normal cells, this conversion of glucose into lactate is normally reserved for low-oxygen conditions. Researchers have now identified a tumor-suppressing protein that helps regulate aerobic glycolysis in breast tumors. HRD1 is an enzyme known to suppress breast cancer proliferation and invasion. Experiments on human breast cancer cells clearly showed that upregulation of HRD1 decreased aerobic glycolysis. and subsequently inhibited breast cancer proliferation and invasion. This effect was found to be mediated by the enzyme PFKP. PFKP downregulation allowed HRD1 to inhibit the aerobic glycolysis and spread of breast cancer cells. These findings point to a new regulatory role for HRD1 and offer a possible target for future breast cancer therapies..."

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.

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:

"Patients with osteoarthritis typically experience progressive cartilage degeneration, joint inflammation, and bony growth around the joints. Treatment of this painful condition remains difficult because the underlying mechanisms aren’t clear, but recent evidence suggests that an increase in aerobic glycolysis, a form of glucose metabolism, may play a role. Aerobic glycolysis is regulated in part by the enzyme hexokinase 2 (HK2), which is upregulated in the joint tissues of patients with osteoarthritis . In addition to participating in glycolysis, HK2 affects cell growth, proliferation, survival, organelle recycling, and death under the influences of various other osteoarthritis-related proteins and pathways. For example, HK2 activity is promoted by the PI3K/Akt pathway, which is activated in osteoarthritis cartilage and HK2 might activate the transcription factor NF-κB to encourage downstream inflammatory processes in joints..."

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