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 immunosuppressive tumor microenvironment (TME) plays essential roles in cancer development and progression. Exosomes mediate crosstalk between tumor cells and other stromal or immune cells in the TME, but how tumor-derived exosomes promote the progression of bladder cancer, one of the most common types of cancer, remains unclear. To find out, researchers recently examined the effects of exosomes extracted from the conditioned medium (CM) of MB49 bladder cancer cells. The researchers found that the cancer-derived exosomes were ingested by mouse macrophages both in vitro and in vivo and that they induced macrophage polarization toward the immunosuppressive M2 phenotype. Exosome-secreting MB49 cells induced tumor growth in mice, but the exosome inhibitor GW4869 reduced tumor growth, macrophage M2 polarization and immunosuppression, confirming the pro-tumor effects of the cancer-derived exosomes..."

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:

"Scientists have uncovered new details about endothelial cell differentiation that could lead to better management of vascular disease. Endothelial cells are often damaged in conditions like coronary artery disease. This damage can be repaired through the transplantation of healthy endothelial cells. But acquiring these cells at the quantities and purity needed for therapeutic transplantation is no easy task. To help solve this problem, the researchers took a closer look at the molecular factors that direct stem cells to adopt an endothelial phenotype. The team started by isolating mononuclear cells from just 1 mL of blood. They later reprogrammed these cells into induced pluripotent stem cells. To accomplish this, they used an optimized, non-integrating protocol – with very good results. The stem cells were then differentiated into endothelial cells, and the researchers tracked gene expression throughout the process..."

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:

"Extracellular vesicles (EVs) are key participants in cell-to-cell communication that exert various effects via the diverse molecular cargoes they carry from their parent cells. However, they also play pathological roles by carrying damage and disease signals from abnormal cells. In cancer, for example, tumor cells secrete EVs that help them evade immune surveillance and target macrophages to create a pro-tumor environment. In turn, tumor-associated macrophages release EVs that target tumor cells to enhance migration and proliferation. Notably, chemo- or radiotherapy can actually increase EV secretion, contributing to immunosuppression and cancer metastasis. In the liver, EV-mediated communication between hepatocytes and macrophages or hepatic stellate cells can exacerbate injury or disease and EV signaling can eventually contribute to insulin resistance..."

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:

"The expression of human genes is partially modulated by epigenetic mechanisms. There is a dramatic epigenetic transformation during transition of embryonic stem cells (ESCs) to specialized cells and the reprogramming of somatic cells to become induced pluripotent stem cells (iPSCs). Aberrant epigenetic changes can contribute to carcinogenesis and other disorders. The histone demethylase Jumonji domain-containing protein-3 (JMJD3) regulates the trimethylation of histone H3 on lysine 27 (H3K27me3), which is an important epigenetic event associated with transcriptional silencing. JMJD3 function has been studied in relation to immune diseases, cancer, and tumor development. Recent studies have suggested that JMJD3 also plays a major role in cell fate determination of pluripotent and multipotent stem cells. JMJD3 specifically enhances self-renewal ability and reduces the differentiation capacity of ESCs and multipotent stem cells..."

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

This presentation was developed by Martha Lopez Yrigoyen. It is intended as a flexible tool for lectures and tutorials for first year students in the Biological and Biomedical Sciences. Diagrams are also encouraged to be used by scientists, science communicators and educators.Not all slides will be useful for everyone or for every occasion. Slides can be adapted for the purpose needed. There are two main activities intended for undergraduate students to engage and deepen their knowledge in the field of stem cells. The first  activity is more general and its aim is to familiarize students with the core concepts in stem cell and regenerative medicine. The second activity is a novel and current example of how induced pluripotent stem cells are being used in cutting edge biomedical research. The two publications suggested for students to read can be swapped for other examples. Presentationislicensed under a Creative Commons Attribution License 4.0https://creativecommons.org/licenses/by/4.0/

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:

"Tribbles homolog 2 (Trib2) is a pseudo serine/threonine kinase that functions as a scaffold or adaptor in many signaling pathways. Trib2 can interact with E3 ubiquitin ligases and affect the protein stability of downstream effectors, controlling transcription, cell proliferation, apoptosis, survival, and differentiation, with effects on metabolism and disease. In contrast to its critical role in cell development and homeostasis, Trib2 is also induced by mitogens and enhances cancer cell proliferation. Its involvement in several hematopoietic cancers and solid tumors makes it a valuable biomarker for cancer diagnosis and treatment. Recent studies have shown that Trib2 also plays a major role in determining the fate of stem cells, which have the potential to self-renew and differentiate into many different cell types. Trib2 may be necessary for colony formation and self-renewal of embryonic stem cells (ESCs), and loss of Trib2 function is associated with ESC differentiation..."

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