No abstract

Background: ERBB4 plays an important role in the etiology and progression of lung cancer. Results: miR-193a-3p suppressed proliferation and invasion and promoted apoptosis in lung cancer cells and xenograft mice by negatively regulating ERBB4. Conclusion: miR-193a-3p exerted an anti-tumor effect by negatively regulating ERBB4 in lung cancer. Significance:This study may open new avenues for future lung cancer therapies.

Drug abuse has spread quickly since reemerging as a national problem in China in the late 1980s. The number of registered drug abusers increased from 70 000 in 1990 to more than one million by the end of 2004. In addition to opioids, abuse of “new” types of drugs including 3,4‐methylenedioxymethamphetamine (MDMA) and ketamine has spread since 1997. Illicit drug trafficking and production have swept most of southern China, and throughout the country drug abuse has caused many problems for both abusers and the community. One major drug‐related problem is the spread of HIV, which has caused major social and economic damage in China. In response, the Chinese government has begun an anti‐drug campaign, including legislative measures to control drug abuse. However, changing the public's attitudes toward drug abusers and breaking the link between drug use and HIV spread are equally important.

MicroRNAs (miRNAs) are short non-coding RNAs of 21–23 nucleotides that play important roles in virtually all biological pathways in mammals and in other multicellular organisms. miR-23a and miR-23b (miR-23a/b) are critical oncomiRs (miRNAs that are associated with human cancers) of gastric cancer, but their detailed roles in the initiation and progression of gastric cancer remain to be elucidated. In this study, we found that miR-23a/b were consistently upregulated in gastric cancer tissues. We then investigated the molecular mechanisms through which miR-23a/b contribute to gastric cancer and identified programmed cell death 4 (PDCD4) as a direct target gene of miR-23a/b. In contrast to the upregulated expression levels of miR-23a/b, PDCD4 protein levels were dramatically downregulated and inversely correlated with miR-23a/b in gastric cancer tissues. Moreover, we observed that cell apoptosis was increased by miR-23a/b inhibitors and decreased by miR-23a/b mimics in gastric cancer cells and that the restoration of PDCD4 expression attenuated the anti-apoptotic effects of miR-23a/b in gastric cancer cells, indicating that PDCD4 is a direct mediator of miR-23a/b functions. Finally, we showed that miR-23a/b significantly suppressed PDCD4 expression and enhanced tumor growth in a gastric cancer xenograft mouse model. Taken together, this study highlights an important role for miR-23a/b as oncomiRs in gastric cancer through the inhibition of PDCD4 translation. These findings may shed new light on the molecular mechanism of gastric carcinogenesis and provide a new avenue for gastric cancer treatment.