MIR-147B Regulated Proliferation and Apoptosis of Gastric Cancer Cells by Targeting CPEB2 Via the PTEN Pathway.

The present study has been performed to illustrate the role and mechanism of microRNA-147b (miR-147b) in the cellular viability and apoptosis of gastric cancer (GC) cells. The GC tissues of 50 patients with complete data and the adjacent tissues were selected from Shanxi Cancer Hospital, and 3 pairs of tissues were randomly selected for microarray detection of high-expressing microRNAs. The expressions of miR-147b were quantified in numerous GC cell lines, i.e., BGC-823, SGC-7901, AGS, MGC-803 and MKN-45, normal tissue cell lines and 50 pairs of gastric cancer tissues. Moreover, two cell lines of miR-147b high-expressing used PCR quantitative analysis were selected for transfection experiments. The differentially expressed miR-147b was screened from 3 pairs of samples by miRNA chip. The expression ofmiR-147b was found highly expressed in gastric cancer tissues of 50 pairs of gastric cancer and adjacent tissues. The miR-147b found in diverse range in each of GC cell line. Therefore, two cell lines, BGC-823 and MGC-803, with relatively high expression levels of miR-147b were selected for further analysis and research. Scratch analysis results showed that compared with miR-147b NC, the miR-147b inhibitor group inhibited GC cell growth and reduced cell migration. The early apoptosis of MGC-803, and BGC-823 cells was enhanced by miR-147b inhibitor. miR-147b inhibitor significantly repressed the proliferation of BGC-823 and MGC-803 cells. Our study showed that the high expression of miR-147b is positively correlated with the occurrence and development of gastric cancer.

Anterior cingulate cortex, insula and amygdala seed-based whole brain resting-state functional connectivity differentiates bipolar from unipolar depression.

OBJECTIVE: The frontal-limbic circuit is hypothesized as sub-serving emotional regulation. We performed whole brain resting-state functional connectivity (rs-FC) analysis by studying the key hubs of frontal-limbic circuit: anterior cingulate cortex (ACC), bilateral insula subregions, bilateral amygdala (Amy) as seeds, separately, to discriminate bipolar depression (BipD) from unipolar depression (UniD). METHODS: We compared seed-based rs-FC of the frontal-limbic seeds with whole brain among 23 BipD participants; 23 age, gender, and depression severity matched patients with UniD, and 23 healthy controls (HCs). We also used support vector machine learning to study classification based on the rs-FC of ACC, bilateral insula subregions, and bilateral Amy seeds with whole brain. RESULTS: BipD showed increased rs-FC between the left ventral anterior insula (vAI) seed and the left anterior supramarginal gyrus (aSMG) and left postcentral gyrus, as well as increased rs-FC between left amygdala seed and the left aSMG when compared to HCs and UniD. Compared to UniD, BipD was associated with increased rs-FC between right dorsal anterior insula seed and right superior frontal gyrus, as well as increased rs-FC between left posterior insula seed and right precentral gyrus and right thalamus. Combined rs-FC of ACC, bilateral insula subregions and bilateral Amy seeds with the whole brain discriminated BipD from UniD with an accuracy of 91.30%. CONCLUSIONS: Rs-FC of the emotional regulation circuit is more widely disturbed in BipD than UniD. Using rs-FC with this circuit may lead to further developments in diagnostic decision-making.

Tanshinones suppress AURKA through up-regulation of miR-32 expression in non-small cell lung cancer.

Tanshinone is the liposoluble constituent of Salia miltiorrhiza, a root used in traditional herbal medicine which is known to possess certain health benefits. Although it is known that tanshinones, including tanshinone I (T1), tanshinone IIA (T2A), and cryptotanshinone (CT), can inhibit the growth of lung cancer cells in vitro, the mechanism under which they act is still unclear. AURKA, an oncogene, encodes a serine-threonine kinase which regulates mitotic processes in mammalian cells. Here, we reported that tanshinones mediate AURKA suppression partly through up-regulating the expression of miR-32. We found that tanshinones could inhibit cell proliferation, promote apoptosis, and impede cell-cycle progression, thus performing an antineoplastic function in non-small cell lung cancer (NSCLC). Additionally, we demonstrated that tanshinones attained these effects in part by down-regulating AURKA, corroborating previous reports. Our results showed that in NSCLC, similar effects were obtained with knock-down of the AURKA gene by siRNA. We also verified that AURKA was the direct target of miR-32. Collectively, our results demonstrated that tanshinones could inhibit NSCLC by suppressing AURKA via up-regulating the expressions of miR-32 and other related miRNAs.