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 myeloid leukemia (AML) is a type of blood and bone marrow cancer with a low survival rate. One reason AML is so deadly is because it can evade the immune system, in part by downregulating proteins like MICA, which normally marks damaged or cancerous cells in the body for immune destruction. To improve treatment prospects, researchers recently searched for molecules that can restore MICA levels in AML cells. They found that the transcription factor KFL4 is involved in MICA expression. In addition, treating cultured AML cells with the KLF4-activating compound APTO253 successfully induced MICA expression, while inhibiting the expression of the cancer gene MYC. These changes made the AML cells more susceptible to being killed by immune cells. Although studies in animals and humans are still needed, these findings reveal that APTO253 can improve immune cells’ ability to detect and kill AML cells and suggest that targeting KFL4/MICA is a promising option for AML 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:

"Tumor cells reprogram cellular energy metabolism to power their rapid proliferation. One important energy source for tumors is the amino acid glutamine, making glutamine metabolism a promising target for tumor treatment. However, glutamine is also important for proper immune cell function. Tumor cells can potentially outcompete immune cells for glutamine, tipping the scales of immunity in their favor. Certain intrinsic signaling programs may also help partition glutamine within tumor cells while causing immune cells to rely more heavily on glucose. Among immune cells, the tumor-induced glutamine shortage reduces the activity of cancer-fighting T effector cells. It may also disrupt the balance of other immune cell types such as macrophages, but it’s unclear whether the net effects are pro- or anti-tumor..."

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:

"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:

"Peptide hormones are important signaling molecules within the body. One such peptide is the secreted protein augurin, which is encoded by the gene Ecrg4, whose expression has been reported in a wide range of human tissues. The product of the gene Ecrg4, the augurin precursor ECRG4, has been predicted to be cleaved to originate different peptides. Augurin is implicated in a variety of processes, including tumorigenesis, inflammation, and infection. It is also involved in the regulation of the hypothalamo-pituitary adrenal axis and in osteoblast differentiation. Augurin is implicated in the modulation of well-known signaling cascades, including NF-kB, PI3K/Akt/mTor, Wnt-beta catenin, and apoptosis pathways, however, the molecular mechanisms underlying its action remain largely unexplored. Given its involvement in health and disease, augurin is an attractive target for the discovery of new therapeutic agents for human pathologies..."

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