CD13 - an important protein for cellular migration.

Cell migration is a fundamental process that involves the coordination of complex biochemical and biomechanical signals to modulate cell morphology by dynamically rearranging cytoskeleton filaments and to cause cellular traction. Slight alteration in this tightly regulated process in a cell could result in a wide variety of pathologies including metastasis of cancer cells. More than 200 proteins are known to be involved in this dynamic process. A new study from University of Connecticut identifies crucial role for a novel protein CD13 in cell to extracellular matrix (ECM) adhesion. This study demonstrates that CD13 controls integrin recycling a major protein family responsible for cellular migration.

https://stke.sciencemag.org/content/12/579/eaav5938?utm_campaign=toc_signaling_2019-04-30&et_rid=17082276&et_cid=2793732

Circadian rhythm and cancer !

It has been known for quite some time that disrupting sleep and other elements of humans' circadian rhythm can harm health. The same is true for the circadian clock of individual cells as well. So a a group of Japanese scientists wondered if disturbing the circadian clock of cancer cells could potentially hurt/weaken or even kill these cancer cells. They were right indeed...! What these researchers reported that a molecule named GO289 targets an enzyme casein kinase 2 that controls the cell's circadian rhythm, shows great clinical promise in halting cancer cells' growth by enabling manipulation of clock protein phosphorylation.

http://advances.sciencemag.org/content/5/1/eaau9060

"Trans-differentiation" approach to treat metastasis

It is well established that de-differentiation in cancer cells lead to increased malignancy and cancer-metastatic potential. Therefore, treating cancer by inducing cancer cell differentiation has been long haunted strategy for cancer biologists with little success in clinic, except few successful examples such as use of all-trans retinoic acid as differentiation therapy for acute promyelocytic leukemia. One of the major impediment underlying failure of various differentiation therapies is due to the dynamic nature of epithelial to mesenchymal transition (EMT) and its reverse (MET) of cancer cells during tumor dissemination and metastatic outgrowth which underscores the possible weakness of epithelial re-differentiation strategies. Here is a breakthrough study that demonstrates with strong body of evidences that cancer cell plasticity can directly be targeted and inhibited by a “trans-differentiation approach”, such as forced adipogenesis. Indeed, these findings using a therapeutic approach to target metastatic cancer cell by inducing them to become adipocytes (fat cells) show a great promise at least in pre-clinical studies. hashtag
https://www.cell.com/action/showPdf?pii=S1535-6108%2818%2930573-7

#tumors hashtag#metastasis hashtag#health