Cten promotes Epithelial-Mesenchymal Transition (EMT) in colorectal cancer through stabilisation of Src.

Cten is an oncogene promoting EMT in many signaling pathways, namely through Snail. We investigated whether Cten function could be mediated through Src. Cten levels were modulated by forced expression in HCT116 and gene knockdown in SW620 CRC (colorectal cancer) cell lines.

Cten promotes epithelial-mesenchymal transition through the post-transcriptional stabilization of Snail.

Cten promotes cell migration however the knowledge of underlying signalling pathways is sparse. We have shown that Cten downregulates E-cadherin, a feature of epithelial to mesenchymal transition (EMT). This prompted us to investigate whether Cten further contributed to EMT processes to regulate cell motility.

Multiple pathways regulate Cten in colorectal cancer without a Tensin switch.

CTEN/TNS4 is a member of the Tensin gene family. It localizes to focal adhesions and induces cell motility. The mechanisms regulating Cten expression are unclear although we have shown regulation by Kras in the colon and pancreas.

Placental morphology in pre-eclampsia and eclampsia and the likely role of NK cells.

Background: Placenta has long been a neglected organ as far as its pathology is concerned. This study is an attempt to observe the morphological features of placentae both gross and microscopic in normal pregnancy, preeclampsia, and eclampsia.

Materials And Methods: A total of 150 placentae were collected; of these, 50 belonged to normal pregnancy, 50 belonged to pre-eclamptic women, and 50 were from patients of eclampsia.