epithelial-mesenchymal transition of metastasis

[@nicochacin4490]

i liked the blue screen at the end, very soothing

[@TheYoubose]

I recon it is 'cathepsin' instead of 'cathespin' at 0.39

[@carolinegronnier6888]

Thank you . This video was really helpful !

[@OmegaPsiPhi0]

Your so gorgeous! 😍 Xx

[@egs8545]

Very helpful, thank you for making this!

[@DaFan86]

awesome video!

[@Mrasboi]

Thank you, Great video!

[@brcarter1111]

I'm not sure you mentioned it, but another important change that occurs with the change into a MSC is the loss of MHC I expression, which is very very bad if you are a cancer cell making this transition

[@johnsnow1235]

Is the reason you say it is bad for a cancer cell making the transition as loss of MHC1 expression leads to NK cell activation resulting in those cancer cells being destroyed, or is it for some other reason?

[@brcarter1111]

@@johnsnow1235 It is quite poorly understood, but that is a potential reason. In human cancers, most loss of MHC I is actually due to epigentic suppression, not mutations that destroy the genes. Some studies have shown that being able to express MHC I gives an enhanced ability to undergo EMT and cause metastasis. Often times, cancer cells can begin re-expressing MHC I after extravasation (leaving the vasculature/lymphatics and entering a new tissue). Some argue this is because it may prevent lysis by NK cells in transit, but then why suppress expression when in transit, when most NK cells are tissue resident? I believe this phenomenon is due to other reasons. I think EMT is not solely responsible for metastasis, but is part of a complex gene program that causes metastasis. Cancer is believed to be a disease caused by microevolution caused by mutation, but metastasis is, in my opinion, far too ordered of a process to be occurring as the result of random mutations.

[@JV-cz6fz]

They also upregulated PD-1 potentially having a way of balancing off some immune survelliance

[@JV-cz6fz]

@@brcarter1111 I wouldn't say EMT is due to random mutations per se but invasion and metastasis is absolutely a hallmark of cancer, an emerging hallmark that I think will be added eventually to the list of hallmarks of cancer is heterogeneity, at some point the tumor is so heterogeneous they act as a kind of organ that cooperates to survive, and even the seeding of metastasis is the result of role compartmentalization, cancer cells will travel as clusters which can help establish the invasion of a distant tissue, because as soon as the cancer arrives at a distant site it has to become epithelial again, therefore it's a question of wether the invading tissue undergoes MET or if the cluster carries with it epithelial cells that hitched a ride. all very interesting stuff. Also genetic instability while a hallmark of cancer is most definitely not enough to explain all of cancer behavior, I think that's sort of implied imo but I could see how some would think inherent genetic instability. Epigenetic alterations are also recognized as a hallmark of cancer, it can be a question if upstream of that genetic instability you're seeing mutation in epigenetic genes, so it would come full circle.

[@crimapogge1377]

Thank you, very clear!

[@nubepegajosa8115]

thaaanks

[@salmatounsi305]

thank you . I want to know is that there is a role of platelets in the primary decrease of E-cad and the expresion and upregulution of N-cad