This study was performed to investigate the role of galectin-1 (Gal-1) in epithelial ovarian cancer (EOC) progression and chemoresistance. Tissue samples from patients with EOC were used to examine the correlation between Gal-1 expression and clinical stage of EOC. The role of Gal-1 in EOC progression and chemoresistance was evaluated in vitro by siRNA-mediated knockdown of Gal-1 or lentivirus-mediated overexpression of Gal-1 in EOC cell lines. To elucidate the molecular mechanisms underlying Gal-1-mediated tumor progression and chemoresistance, the expression and activities of some signaling molecules associated with Gal-1 were analyzed. We found overexpression of Gal-1 in advanced stages of EOC. Knockdown of endogenous Gal-1 in EOC cells resulted in the reduction in cell growth, migration, and invasion in vitro, which may be caused by Gal-1's interaction with H-Ras and activation of the Raf/extracellular signal-regulated kinase (ERK) pathway. Additionally, matrix metalloproteinase-9 (MMP-9) and c-Jun were downregulated in Gal-1-knockdown cells. Notably, Gal-1 overexpression could significantly decrease the sensitivities of EOC cells to cisplatin, which might be ascribed to Gal-1-induced activation of the H-Ras/Raf/ERK pathway and upregulation of p21 and Bcl-2. Taken together, the results suggest that Gal-1 contributes to both tumorigenesis and cisplatin resistance in EOC. Thus, Gal-1 is a potential therapeutic target for EOC.

It is increasingly clear that microRNAs (miRNAs) play an important role in many diseases, including tumorigenesis. However, the mechanisms by which miRNAs regulate bladder cancer development remain poorly understood. Here, we evaluated the expression of microRNA‐203 (miR‐203) in bladder cancer tissues using real‐time PCR, and defined the target genes and biologically functional effect using luciferase reporter assay, flow cytometry and western blot analysis. We first verified that the expression of miR‐203 was decreased in bladder cancer tissues. Moreover, ectopic expression of miR‐203 promoted the apoptosis of human bladder cancer cell lines and inhibited cell proliferation, whereas its depletion increased cell growth. We further verified that miR‐203 directly targeted 3′‐untranslated region of the bcl‐w gene, and decreased its expression in vitro and in vivo. Western blot analysis also showed that the expression level of miR‐203 was negatively correlated with bcl‐w level in tumor tissues. These data suggest an important role for miR‐203 in the molecular etiology of bladder cancer and implicate the potential application of miR‐203 in bladder cancer therapy.

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Sentiment Analysis is an important research direction of natural language processing, and it is widely used in politics, news and other fields. Word embeddings play a significant role in sentiment analysis. The existing sentiment embeddings methods directly embed the sentiment lexicons into traditional word representation. This sentiment representation methods can only differentiate the sentiment information of different words, not the same word in different contexts, so it cannot provide accurate sentiment information for word in different contexts. This paper proposes sentiment concept to solve the problem. First, we found the optimal sentiment concept of words in Microsoft Concept Graph according to the context of words. Then we obtained the sentiment information of words under optimal sentiment concept from the multi-semantics sentiment intensity lexicon which we constructed in this paper to achieve accurate embedding of sentiment information and provide more accurate semantics and sentiment representation for words. Finally, we combined two refined word embeddings methods to achieve a more comprehensive word representation. Compared with traditional and sentiment embeddings methods on six representative datasets, the validity of the word embeddings method based on sentiment concept proposed in this paper is verified.INDEX TERMS Deep learning, sentiment analysis, sentiment concept, word embeddings.

The aim of the current study was to profile c-Myc, standard CD44 (CD44s), CD44v6, cyclin D1, survivin, MMP-7 and VEGF expression patterns in different gastric samples and to elucidate their relevance for Wnt, NF-kappaB and/or Stat3 activation using multiple experimental approaches. The results revealed that 87.1% (27/31) of gastric cancers and 8.7% (2/23) of noncancerous lesions (chronic gastritis and intestinal metaplasia) showed Wnt activation (Wnt(+)) that was closely related to the expression of the seven genes. Some Wnt(-) noncancerous lesions also expressed the above-mentioned genes, higher frequencies of survivin (7/8), VEGF (7/8), cyclin D1 (6/8) and c-Myc (5/8) but not CD44s (2/8), CD44v6 (3/8) and MMP-7 (2/8) being detected in the NF-kappaB(+) samples. Stat3 was activated in 37/54 gastric tissues, and in 3/4 VEGF, 4/6 c-Myc, 4/8 survivin, 2/4 MMP-7, 1/2 CD44v6, and 4/9 cyclin D1(+) but Wnt(-)/NF-kappaB(-) samples. These findings showed a close correlation in GCs between Wnt, NF-kappaB and Stat3 signaling and expression of the seven genes, the importance of NF-kappaB and Stat3 activation in regulating c-Myc, survivin, cyclin D1 and VEGF in noncancerous lesions, and the potential coordinative effects of these three signalings on GC formation presumably by promoting the transcription of their common target genes.

The peroxisome proliferator-activated receptor-γ (PPAR-γ) coactivator-1β (PGC-1β) is a well-established regulator of mitochondrial biogenesis. However, the underlying mechanism of PGC-1β action remains elusive. This study reveals that knockdown of endogenous PGC-1β by short-hairpin RNA (shRNA) leads to a decrease in the expression of mammalian target of rapamycin (mTOR) pathway-related genes in MDA-MB-231 cells. After knockdown of PGC-1β, phosphorylation of AMP-activated protein kinase (AMPK), phosphorylation of Rictor on Thr1135, Raptor and S6 protein was inhibited. However, Akt phosphorylation on Ser473 was upregulated and cell apoptosis occurred. In particular, we demonstrate that the levels of PGC-1β and mTOR correlated with overall mitochondrial activity. These results provide new evidence that cell apoptosis is orchestrated by the balance between several signaling pathways, and that PGC-1β takes part in these events in breast cancer cells mediated by the mTOR signaling pathway.

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