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Long noncoding RNAs (lncRNAs) are a group of nonprotein coding transcripts that play a critical role in cancer progression. However, the role of lncRNA in metformin-induced inhibition of cell growth and its biological function in gastric cancer remain largely unknown. In this study, we identified an oncogenic lncRNA, Loc100506691, the expression of which was decreased in gastric cancer cells with metformin treatment. Moreover, Loc100506691 was significantly overexpressed in gastric cancer compared with adjacent normal tissues (p < 0.001), and high Loc100506691 expression was significantly correlated with poor survival of patients with gastric cancer. Additionally, Loc100506691 knockdown could significantly suppress gastric cancer cell growth in vitro, and ectopic Loc100506691 expression accelerated tumor growth in an in vivo mouse model. Analysis of the cell cycle revealed that Loc100506691 knockdown induced cell cycle arrest at the G2/M phase by impairing cell entry from the G2/M to G1 phase. Loc100506691 negatively regulated CHAC1 expression by modulating miR-26a-5p/miR-330-5p expression, and CHAC1 knockdown markedly attenuated Loc100506691 knockdown-induced gastric cancer cell growth and motility suppression. We concluded that anti-proliferative effects of metformin in gastric cancer may be partially caused by suppression of the Loc100506691-miR-26a-5p/miR-330-5p-CHAC1 axis., Graphical abstract, This new signaling pathway broadens our understanding of the mechanism and anticancer potential of metformin in the treatment of gastric cancer. Our findings showed anti-proliferative effects of metformin in gastric cancer may be caused by suppression of the novel Loc100506691-CHAC1 axis.

Demand for the detection of estradiol, which is a naturally occurring hormone, has been increasing. Gold nanoparticle-based colorimetric aptasensors have been developed for estradiol detection; however, the long sequence of aptamers due to the formation of the secondary structure likely affects the sensitivity of the aptasensors. Herein, a sensitive colorimetric biosensor is developed for label-free detection of estradiol by using an estradiol-specific split aptamer. The results demonstrate that a superior response is observed when a split aptamer with a high free energy of the secondary structure (ΔG > -3 kcal/mol) is used, in comparison to that observed using a split aptamer with a low free energy of the secondary structure (ΔG < -3 kcal/mol) at 27°C. After selecting the appropriate split aptamer, the standard calibration curve obtained for estradiol has a detection limit of 6.7 nM, with a linear range of 6.7 nM - 66.7 μM in the logarithmic scale. Furthermore, this assay is sensitive, easy-to-operate, inexpensive, and non-time-consuming (provides results within 50 min), thereby showing potential for clinical applications (detection of other small molecular targets).

With the increasing development of big data analytics, more and more researchers have started to apply related technologies to various business projects. However, so far most of these projects have only considered the data of the shop, such as daily visitor estimation or daily sales estimation. The substantial promotion of the shop and the scheduling of promotion manpower, however, remain topics that have rarely been discussed. Therefore, this study proposes a new query to discuss these two issues simultaneously. In this new query, we conduct the following steps: (1) Using the borrowed records of the bicycle sharing system for the location of the query shop, we find out what other locations are most frequently visited by people in the vicinity of the query shop, and consider these locations as key sources of customers; (2) Using NNs to predict the traffic at these key sources; (3) Using GA to find out how to schedule the staff to distribute flyers at these key sources if the shop needs to have such arrangement. The final experimental simulation verifies the effectiveness of the proposed method.

Lung cancer is the most prevalent types of cancer and the leading cause of cancer-related deaths worldwide. Among all cancers, lung cancer has the highest incidence, accompanied by a high mortality rate at the advanced stage. Favorable prognostic biomarkers can effectively increase the survival rate in lung cancer. Our results revealed FAM83A (Family with sequence similarity 83, member A) overexpression in lung cancer tissues compared with adjacent normal tissues. Furthermore, high FAM83A expression was closely associated with poor lung cancer survival. Here, through siRNA transfection, we effectively inhibited FAM83A expression in the lung cancer cell lines H1355 and A549. FAM83A knockdown significantly suppressed the proliferation, migration, and invasion ability of these cells. Furthermore, FAM83A knockdown could suppress Epidermal growth factor receptor (EGFR)/Mitogen-activated protein kinase (MAPK)/Choline kinase alpha (CHKA) signaling activation in A549 and H1355. By using a bioinformatics approach, we found that FAM83A overexpression in lung cancer may result from miR-1-3p downregulation. In summary, we identified a novel miR-1-FAM83A axis could partially modulate the EGFR/choline phospholipid metabolism signaling pathway, which suppressed lung cancer growth and motility. Our findings provide new insights for the development of lung cancer therapeutics.

Colorectal carcinoma (CRC) is one of the most prevalent cancers worldwide and has a high mortality rate. Long noncoding RNAs (lncRNAs) have been noted to play critical roles in cell growth, cell apoptosis, and metastasis in CRC. This study determined that LOC441461 expression was significantly higher in CRC tissues than in adjacent normal mucosa. Pathway enrichment analysis of LOC441461-coexpressed genes revealed that LOC441461 was involved in biological functions related to cancer cell growth and motility. Knockdown of the LOC441461 expression significantly suppressed colon cancer cell growth by impairing cell cycle progression and inducing cell apoptosis. Furthermore, significantly higher LOC441461 expression was discovered in primary colon tumors and metastatic liver tumors than in the corresponding normal mucosa, and LOC441461 knockdown was noted to suppress colon cancer cell motility. Knockdown of LOC441461 expression suppressed the phosphorylation of MLC and LIMK1 through the inhibition of RhoA/ROCK signaling. Overall, LOC441461 was discovered to play an oncogenic role in CRC cell growth and motility through RhoA/ROCK signaling. Our findings provide new insights into the regulation of lncRNAs and their application in the treatment of colon cancer

Background Colorectal cancer (CRC) is one of the most common cancers and causes of cancer-related death worldwide. In patients with CRC, metastasis is a crucial problem that leads to treatment failure and is the primary cause of the lethality of colon cancer. Long noncoding RNAs (lncRNAs) have recently emerged as critical molecules in the development, cell growth, apoptosis, and metastasis of CRC. Method We investigated the transcriptome profiles of human lncRNAs in the primary tumor tissues and in the corresponding normal mucosa of two patients with CRC by using a microarray approach. The expression levels of lncRNAs were verified in colon cancer by real-time PCR. Using bioinformatics approach to illustrate putative biological function of Linc00659 in colon cancer. The effects of Linc00659 on cell growth, proliferation, cell cycle and apoptosis were studies by in vitro assays. Results Our data revealed that compared with adjacent normal tissues, 201 lncRNAs were deregulated (fold change ≥ 4 or ≤ 0.25) in CRC tissues. Among them, the expression levels of Linc00659 were significantly increased in colon cancer, and high expression levels were correlated with poor survival in patients with CRC. Bioinformatics analysis results indicated that Linc00659 was significantly coexpressed with cycle-related genes in CRC. Linc00659 expression knockdown could significantly suppress colon cancer cell growth by impairing cell cycle progression. In addition, our results showed that Linc00659 expression knockdown could accelerate cell apoptosis in colon cancer cells treated with chemotherapy drugs. Meanwhile, our results also demonstrated that silencing of Linc00659 expression leads to cell growth inhibition and induced apoptosis, possibly by suppressing PI3K-AKT signaling in colon cancer. Conclusion Linc00659 is a novel oncogenic lncRNA involved in colon cancer cell growth by modulating the cell cycle. Our findings give an insight into lncRNA regulation and provide an application for colon cancer therapy. Electronic supplementary material The online version of this article (10.1186/s12943-018-0821-1) contains supplementary material, which is available to authorized users.

Figure S3. Examination of the subcellular fractionation localization of Linc00659 in CRC cell lines. After nuclear and cytosolic separation, total RNA from Lovo, HCT116, HT29, SW620 and DLD-1 cells underwent RT and real-time PCR. GAPDH was used as a cytosol marker (A) and U6 was used as a nucleus marker (B). (C) RNA expression levels of Linc00659 candidates in the nucleus and cytoplasm were measured by real-time PCR, respectively. CRC, colorectal cancer; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; PCR, polymerase chain reaction. (DOCX 109Â kb)

Figure S2. Stable knockdown of Linc00659 expression with shLinc00659#2 suppressed HCT116 cell growth. (A) The expression levels of Linc00659 were examined in HCT116 cells with stable shLinc00659#2 knockdown. (B) and (C) The cell proliferation and colony formation assays were performed: (D) graph illustrating quantified values. (E) The effects of Linc00659 knockdown on anchorage-independent growth of HCT116 were examined by a soft agar formation assay: (F) graph illustrating quantified values. Data are reported as the number of colonies relative to the control (means Âą standard deviation). (DOCX 205Â kb)

Figure S1. Knockdown of Linc00659 expression with siRNA suppressed growth of colon cancer cells (A)-(D) The expression levels of Linc00659 were examined after transfection of Lovo, LS174T, DLD-1 and SW620 with siRNA. (E)-(H) After transient transfection of Lovo, LS174T, DLD-1 and SW620 cells with si-Linc00659, cell proliferation was examined; the graph shows quantified values. (DOCX 124Â kb)

MicroRNAs (miRNAs) are small non-coding RNAs that have crucial regulatory functions in carcinogenesis. miR-324-5p and miR-324-3p are generated from the same hairpin RNA structure, however, both are diverse in their direct target genes and expression levels. We report that expression of miR-324-5p and -3p was frequently observed to be either up-regulated or down-regulated, and the selection preference of miR-324 for 5p and 3p arms significantly varied in various types or human cancer. Overexpression of miR-324-5p or -3p suppressed growth and invasion of breast cancer cells. Overexpression of miR-324-5p reduced the growth and invasive abilities of colorectal cancer cells, whereas miR-324-3p suppressed colorectal cancer cell invasion but did not influence cell growth. We conclude that miR-324-5p and miR-324-3p might have distinct biological functions, further complicating the regulatory network in human cancer. Therefore, the arm selection preference of miR-324 may be a method for modulating its function.