No abstract

Background: The role of Notch signalling in human epithelial cancers is of immense interest. In this study, we examine the interplay between Notch signalling and RhoC, a well-established molecular factor in metastasis. By linking the function of Notch and RhoC, we further strengthen the notion that there is a pro-oncogenic role of Notch signalling in human cervical cancers. Methods: RhoC protein expression in cervical carcinoma cell lines was assessed by western blotting. Using CaSki and SiHa cells (cervical carcinoma cells lines), we show that RhoC contributes to wound healing, invasion and migration, anoikis resistance, colony formation, in vitro tube formation and tumour formation. Immunohistochemical studies were carried out to assess the co-expression of RhoC, pAkt and Notch1 in clinical sections. Results: An assessment of the changes associated with epithelial-to-mesenchymal transition (EMT) shows that both Notch1 and RhoC have similar phenotypic contribution to EMT. Rho activity assessment on Notch1 inhibition with DAPT shows decreased RhoC activity. We further show that constitutively active RhoC rescues the phenotypic effect of Notch1 inactivation, and a comparison of Notch1 with RhoC expression shows an overlap between the two proteins in the same areas of the tissue. Conclusion: This study has provided evidence to suggest that RhoC is an effector of Notch1 in cervical carcinoma.

One of Nature's gifts to mankind is mesenchymal stem cells (MSC's). They are multipotent in nature and are present literally in every tissue. Since, they possess certain characteristics of stem cells such as self-renewal and differentiation they are known to be one of the key players in normal tissue homeostasis. This novel function of mesenchymal stem cells has been explored by scientists in the field of regenerative medicine. This review gives an insight of the various sources of mesenchymal stem cells available for tissue engineering with regard to tendon and ligament and the mechanism involved during regeneration.

Late stage detection of COVID-19 disease pathogenesis induced by SARS-CoV-2 infection may prove to be fatal to the infected patients with the severity increasing, if inhibition of differentiation of hematopoietic endothelial progenitor cells, or their sustained deficiency, is not reversed. Antiviral drug treatments of such individuals need not necessarily resuscitate from a severe impairment of normal angiogenesis of the vascular endothelium. The virus targets the endothelial progenitor cells which co-express the hematopoietic stem cell marker CD34 and the angiotensin converting enzyme 2 (ACE2), latter being the host receptor for this pathogen. There is not an apparent segregation of CD34 and ACE2 antigens, strongly implicating inhibition of differentiation of virus infected progenitor cells. The embattled clinical condition of SARS-CoV-2 infected patients may well require a dual-mode endothelial progenitor cellular infusion and antiviral drug molecular therapies to stage a rapid clinical recovery. Umbilical cord blood derived CD34+ progenitor cells are the most optimal for rapid availability, harvesting and infusion into the severely ill infected patients, who are most likely to be non-responsive to solely antiviral drug treatments. This is about rapidly prepared allogeneic cell infusion therapy and not autologous cell transplantation which is impractical for these relatively acute and short-term conditions and treatments of SARS-CoV-2 infections. A combination progenitor cell and antiviral drug treatment is suggested for recovery and maintenance of normal angiogenesis of infected patients who may otherwise not survive. Hence the concept and its basis discussed needs to be urgently advanced to translation stage.