In BMC Cancer this week, researchers in China report that microRNA-182 plays a role in metastasis of hepatocellular carcinoma. The team analyzed miR-182 expression in 86 paired samples of hepatocellular carcinoma and normal tissue, and found that the microRNA was overexpressed in cancer tissue compared to normal tissue. That overexpression was correlated with underexpression of the metastasis supressor 1 gene as well as intrahepatic metastasis and poor prognosis of patients. "There was a negative correlation between miR-182 and MTSS1 expression both in HCC tissues and HCC cell lines," the authors write. "Furthermore, the up-regulation of miR-182 resulted in the down-expression of MTSS1 and increased invasive potential of HUH-1, and reverse results were also confirmed when the expression of miR-182 was inhibited."
Also in BMC Cancer this week, researchers in Canada report that cyclophilin 40 — co-chaperone of heat shock protein-90 — promotes the viability of ALK-positive anaplastic large cell lymphoma. The team knocked down the oncoprotein NPM-ALK and transcription factor JunB in ALK-positive ALCL cell lines, and found that NPM-ALK promoted the transcription of Cyp40 and binding protein FKBP52, while JunB promoted Cyp40 transcription only. The researchers also observed reduced viability of the cancer cells with Cyp40 knock-down. "This is the first study demonstrating that the expression of immunophilin family co-chaperones is promoted by an oncogenic tyrosine kinase," the authors write. "Moreover, this is the first report establishing an important role for Cyp40 in lymphoma."
Finally in BMC Cancer this week, researchers in South Korea report that snake venom toxin induces apoptosis in colon cancer cells through the upregulation of ROS- and JNK-mediated death receptor expression. The team applied venom from the Vipera lebetina turanica to colon cancer cell lines and found that it inhibited the growth of colon cancer cells. In addition, they found that the expression of death receptor 4 and death receptor 5 was increased after treatment with venom, and knock-down of DR4 and DR5 reversed the venom's effect. "Snake venom toxin also induced JNK phosphorylation and ROS generation, however, pretreatment of JNK inhibitor and ROS scavenger reversed the growth inhibitory effect of snake venom toxin, and reduced the snake venom toxin-induced upregulation of DR4 and DR5 expression," the authors write.