<i>hsa-miR-29c</i>and<i>hsa-miR-135b</i>differential expression as potential biomarker of gastric carcinogenesis

Vidal, Amanda Ferreira; Cruz, Aline; Magalhães, Leandro; Pereira, Adenilson Leão; Anaissi, Ana Karyssa Mendes; Alves, Nélisson C F; Albuquerque, Paulo J B S; Burbano, Rommel Rodrı́guez; Demachki, Sâmia; Ribeiro-dos-Santos, Ândrea

doi:10.3748/wjg.v22.i6.2060

Cited by 32 publications

(39 citation statements)

References 51 publications

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“…Some findings have suggested that there is an elevation in miR-135b expression in clinical samples compared with the corresponding epithelium; the average expression of miR-135b in GC tissues was notably higher than in the normal epithelium (25). Moreover, hsa-miR-135b has been identified as a promising biomarker for gastric carcinogenesis because its expression has been found to be up-regulated in gastric lesions compared with normal gastric mucosa and intestinaltype gastric adenocarcinoma samples (17). A previous study concluded that MST1 and cyclophilin D expressions were notably reduced in gemcitabine-resistant pancreatic cancer tissues and cell lines (24).…”

Section: Discussionmentioning

confidence: 99%

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Poor expression of microRNA‐135b results in the inhibition of cisplatin resistance and proliferation and induces the apoptosis of gastric cancer cells through MST1‐mediated MAPK signaling pathway

Zhou

Chen

2018

FASEB j.

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Gastric cancer (GC) has been classified as the fourth leading cause of cancer‐related deaths worldwide. Due to their ability to suppress the expression of target genes, microRNAs (miRNAs) are listed as one of the key elements involved in the formation and development of tumors. This study was therefore conducted to investigate the effects of microRNA‐135b (miR‐135b) on cisplatin [ds‐diamminedichloroplatinum (CDDP)] resistance of GC cells through the MAPK signaling pathway by targeting mammalian ste20‐like kinase 1 (MST1). A microarray‐based gene expression analysis was performed to screen the GC‐related differentially expressed genes. The 3‐[4,5‐dimethylthiazol‐2‐yl]‐2,5 diphenyl tetrazolium bromide assay was performed to determine the sensitivity of GC cells to CDDP. The bioinformatics database and dual lucif erase reporter gene assay were used to check whether MST1 was a direct target gene of miR‐135b. GC cell lines were prepared with high CDDP resistance, after which they were cultured and transfected respectively, followed by the administration of transfected cells into nude mice and subsequent treatment with CDDP in an attempt to identify the underlying mechanisms and functions of miR‐135b in relation to MST1 in GC progression. The results were highly indicative of the crucial role played by MST1 in the development of GC and the sensitivity of GC to CDDP. miR‐135b was found to regulate MST1, which in turn had an impact on the development of GC. MKN28 was observed to be most sensitive to CDDP, whereas MKN45 presented with the poorest sensitivity to CDDP. Furthermore, the down‐regulation of miR‐135b resulted in inactivation of the MAPK signaling pathway; increased the expression of MST1 and Bax; and decreased expression of p‐p38MAPK, p‐ERKl/2, P‐glycoprotein, p38MAPK, ERK1/2, multidrug resistance protein 1, multidrug resistance‐associated protein 1, lung resistance‐related protein, and Bcl‐2, thus inhibiting CDDP resistance of GC cells. The down‐regulation of miR‐135b also restrained cell proliferation and induced the apoptosis rate of GC cells. In summary, the results of this study showed that the down‐regulation of miR‐135b induced apoptosis, and it inhibited proliferation and CDDP resistance of GC cells by inactivating the MAPK signaling pathway and increasing the expression of MST1.—Zhou, J., Chen, Q. Poor expression of microRNA‐135b results in the inhibition of cisplatin resistance and proliferation and induces the apoptosis of gastric cancer cells through MST1‐mediated MAPK signaling pathway. FASEB J. 33, 3420–3436 (2019). http://www.fasebj.org

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Section: Discussionmentioning

confidence: 99%

“…An increasing number of studies suggest that a correlation exists between MST1, miR-135b, and the MAPK signaling pathway with GC (16)(17)(18). However, the exact mechanism of the interaction has yet to be thoroughly investigated.…”

Section: Methodsmentioning

confidence: 99%

Poor expression of microRNA‐135b results in the inhibition of cisplatin resistance and proliferation and induces the apoptosis of gastric cancer cells through MST1‐mediated MAPK signaling pathway

Zhou

Chen

2018

FASEB j.

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“…Increasing studies have revealed that the dysregulation of miRNAs is strongly associated with the tumorigenesis and progression of cancers, including GC [16-18]. Additionally, miRNAs have been reported to be used as biomarkers of diagnosis [19] and prognosis [20, 21] in GC.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of microRNA-376a in Gastric Cancer and Association with Poor Prognosis

Zhang¹,

Ma²,

Wu³

et al. 2018

Cell Physiol Biochem

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Background/Aims: MicroRNAs have a significant role in the tumorigenesis and progression of cancers, including gastric cancer (GC). Our study aimed to identify a novel biomarker to predict the prognosis of patients with GC. Methods: The GC microarray dataset, GSE28700, was downloaded from the Gene Expression Omnibus (GEO) database and screened for differentially expressed miRNAs (DEMs). The downregulation of miR-376a expression was verified in GC cell lines and 82 paired GC tissues by performing RT-qPCR and the correlation between its expression and clinicopathological characteristics was also explored. The target genes of miR-376a were predicted using TargetScan7.1, miRDB, and DIANA website tools. A functional enrichment analysis was performed to explore the biological role of the common target genes. Results: Bioinformatics analysis found that miR-376a was downregulated in GC tissues. Compared with the control group, RT-qPCR results showed that the expression of miR-376a in GC cell lines and tissues were also significantly decreased. The expression of miR-376a was statistically associated with T and N stage. Survival analysis with Kaplan–Meier showed that GC patients in the low expression group had a poorer prognosis than those in the high expression group (median survival of 26.4 and 46.9 months, respectively). Univariate and multivariate analysis demonstrated that low miR-376a expression was an independent prognostic marker for poor survival. Functional enrichment analysis indicated that the common targets genes were involved in cell–cell communication, VEGF and mTOR1-mediated signaling, and epithelial-to-mesenchymal transition (EMT). Conclusion: The results suggest that miR-376a could play an important role in the tumorigenesis and progression of GC and act as a novel therapeutic target and prognostic indicator in patients with GC.

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“…Only around 2% of all transcripts (mRNA) are translated into protein, and mounting evidence suggests that the noncoding transcripts (ncRNA), such as short RNA, miRNA, piRNA and more, are as important as mRNAs. For example, micro‐RNA hsa‐miR‐29c is progressively downregulated according to the pathological stages: normal gastric mucosa, nonatrophic chronic gastritis, intestinal metaplasia, and intestinal‐type gastric adenocarcinoma . The DNA methyltransferase 3A, whose expression is increased in gastric cancer, has been implicated.…”

Section: Insights Into the Role Of Noncoding Rnasmentioning

confidence: 99%

“…For example, micro-RNA hsa-miR-29c is progressively downregulated according to the pathological stages: normal gastric mucosa, nonatrophic chronic gastritis, intestinal metaplasia, and intestinal-type gastric adenocarcinoma. 59 The DNA methyltransferase 3A, whose expression is increased in gastric cancer, has been implicated. The upregulation of hsa-miR-135b hints at a function as an onco-miR by acting through its two targets KLF4 and APC.…”

Section: Insights Into the Role Of Noncoding Rnasmentioning

confidence: 99%

Pathogenesis of Helicobacter pylori infection

et al. 2016

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Helicobacter pylori is estimated to infect more than half of the worlds human population and represents a major risk factor for chronic gastritis, peptic ulcer disease, MALT lymphoma, and gastric adenocarcinoma. H. pylori infection and clinical consequences are controlled by highly complex interactions between the host, colonizing bacteria, and environmental parameters. Important bacterial determinants linked with gastric disease development include the cag pathogenicity island encoding a type IV secretion system (T4SS), the translocated effector protein CagA, vacuolating cytotoxin VacA, adhesin BabA, urease, serine protease HtrA, secreted outer membrane vesicles, and many others. The high quantity of these factors and allelic changes in the corresponding genes reveals a sophisticated picture and problems in evaluating the impact of each distinct component. Extensive work has been performed to pinpoint molecular processes related to H. pylori-triggered pathogenesis using Mongolian gerbils, mice, primary tissues, as well as novel in vitro model systems such as gastroids. The manipulation of host signaling cascades by the bacterium appears to be crucial for inducing pathogenic downstream activities and gastric disease progression. Here, we review the most recent advances in this important research area.

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hsa-miR-29candhsa-miR-135bdifferential expression as potential biomarker of gastric carcinogenesis

Abstract: Our results provide evidence of epigenetic alterations in non-atrophic chronic gastritis and intestinal metaplasia and suggest that hsa-miR-29c and hsa-miR-135b are promising biomarkers of gastric carcinogenesis.

Cited by 32 publications

References 51 publications

Poor expression of microRNA‐135b results in the inhibition of cisplatin resistance and proliferation and induces the apoptosis of gastric cancer cells through MST1‐mediated MAPK signaling pathway

Poor expression of microRNA‐135b results in the inhibition of cisplatin resistance and proliferation and induces the apoptosis of gastric cancer cells through MST1‐mediated MAPK signaling pathway

Downregulation of microRNA-376a in Gastric Cancer and Association with Poor Prognosis

Pathogenesis of Helicobacter pylori infection

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