MicroRNA‑665 regulates the proliferation, apoptosis and adhesion of gastric cancer cells by binding to cadherin 3

Fang, Xing; Bai, Yangqiu; Zhang, Lida; Ding, Song‐Ze

doi:10.3892/ol.2021.12755

Cited by 3 publications

(1 citation statement)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Weaker ECM adhesion of P-cadherin depleted IEC could reflect the accelerated remodeling of matrix adhesion complexes contributing to the enhanced collective cell migration. Our finding of inhibited ECM adhesion in P-cadherin deficient IEC is consistent with previously published evidence obtained in breast, gastric and ovarian cancer cells [101][102][103], although the mechanisms of such reduced adhesion remain to be explored. Lower ECM adhesion of P-cadherin-depleted breast and ovarian cancer cells is accompanied by the decreased expression of α6, β1 and β4 integrin subunits [102,103].…”

Section: Discussionsupporting

confidence: 92%

P-Cadherin Regulates Intestinal Epithelial Cell Migration and Mucosal Repair, but Is Dispensable for Colitis Associated Colon Cancer

Naydenov

Lechuga

Zalavadia

et al. 2022

Cells

View full text Add to dashboard Cite

Recurrent chronic mucosal inflammation, a characteristic of inflammatory bowel diseases (IBD), perturbs the intestinal epithelial homeostasis resulting in formation of mucosal wounds and, in most severe cases, leads to colitis-associated colon cancer (CAC). The altered structure of epithelial cell-cell adhesions is a hallmark of intestinal inflammation contributing to epithelial injury, repair, and tumorigenesis. P-cadherin is an important adhesion protein, poorly expressed in normal intestinal epithelial cells (IEC) but upregulated in inflamed and injured mucosa. The goal of this study was to investigate the roles of P-cadherin in regulating intestinal inflammation and CAC. P-cadherin expression was markedly induced in the colonic epithelium of human IBD patients and CAC tissues. The roles of P-cadherin were investigated in P-cadherin null mice using dextran sulfate sodium (DSS)-induced colitis and an azoxymethane (AOM)/DSS induced CAC. Although P-cadherin knockout did not affect the severity of acute DSS colitis, P-cadherin null mice exhibited faster recovery after colitis. No significant differences in the number of colonic tumors were observed in P-cadherin null and control mice. Consistently, the CRISPR/Cas9-mediated knockout of P-cadherin in human IEC accelerated epithelial wound healing without affecting cell proliferation. The accelerated migration of P-cadherin depleted IEC was driven by activation of Src kinases, Rac1 GTPase and myosin II motors and was accompanied by transcriptional reprogramming of the cells. Our findings highlight P-cadherin as a negative regulator of IEC motility in vitro and mucosal repair in vivo. In contrast, this protein is dispensable for IEC proliferation and CAC development.

show abstract

Section: Discussionsupporting

confidence: 92%

P-Cadherin Regulates Intestinal Epithelial Cell Migration and Mucosal Repair, but Is Dispensable for Colitis Associated Colon Cancer

Naydenov

Lechuga

Zalavadia

et al. 2022

Cells

View full text Add to dashboard Cite

show abstract

A novel circular RNA, circMAML3, promotes tumor progression of prostate cancer by regulating miR-665/MAPK8IP2 axis

Zhenhao,

Ru,

Xiaofeng

et al. 2023

Cell Death Discov.

View full text Add to dashboard Cite

Many studies have now demonstrated that circRNAs are aberrantly expressed in cancer and are involved in the regulation of malignant tumor progression. However, the role of circMAML3 (hsa_circ_0125392) in prostate cancer has not been reported. circMAML3 was selected from public data through screening. The circMAML3 circular characterization was performed using Sanger sequencing, agarose gel electrophoresis assay, RNase R assay and actinomycin D assay. The expression of circMAML3 in prostate cancer tissues and cells was detected by qRT-PCR. In vivo and in vitro experiments were conducted to investigate the biological functions of circMAML3 in prostate cancer. Finally, the underlying mechanism of circMAML3 was revealed by qRT-PCR, luciferase reporter assay, miRNA Pulldown, RNA immunoprecipitation, western blotting, and rescue assay. Compared to normal prostate tissue and prostate epithelial cells, circMAML3 is highly expressed in prostate cancer tissues and cell lines. CircMAML3 overexpression promotes prostate cancer proliferation and metastasis, while knockdown of circMAML3 exerts the opposite effect. Mechanistically, circMAML3 promotes prostate cancer progression by upregulating MAPK8IP2 expression through sponge miR-665. Our research indicates that circMAML3 promotes prostate cancer progression through the circMAML3/miR-665/MAPK8IP2 axis. circMAML3 and MAPK8IP2 are upregulated in prostate cancer expression and play an oncogenic role, whereas miR-665 is downregulated in prostate cancer and plays an oncogenic role. Therefore, CircMAML3 may be a potential biomarker for prostate cancer diagnosis, treatment and prognosis.

show abstract

Function of hsa_circ_0006646 as a competing endogenous RNA to promote progression in gastric cancer by regulating the miR-665–HMGB1 axis

Qin¹,

Zhen²,

Wang³

et al. 2023

J Gastrointest Oncol

View full text Add to dashboard Cite

Background Mounting evidences indicate that circular RNAs (circRNAs) are a novel class of non-coding RNAs and play vital roles in the tumorigenesis and aggressiveness including gastric cancer (GC). Nevertheless, the precise functions and underlying mechanisms of circRNAs in GC remain largely unknown. Methods The Gene Expression Omnibus (GEO) data set GSE163416 was analyzed to screen the key circRNAs in GC. hsa_circ_0006646 was chosen for further study. GC tissues and matched adjacent normal gastric mucosal epithelial tissues were obtained from the Fourth Hospital of Hebei Medical University. The expressions of hsa_circ_0006646 was detected using quantitative real-time polymerase chain reaction (qRT-PCR). hsa_circ_0006646 was knocked down to identify its effects on GC cells. Bioinformatics algorithms were analyzed to predict the microRNA (miRNAs) potentially sponged by hsa_circ_0006646 and its target genes. Fluorescence in situ hybridization (FISH) was conducted to determine the subcellular location of hsa_circ_0006646 and the predicted miRNA. Then, qRT-PCR, luciferase reporter assay, radioimmunoprecipitation assay, Western blotting, and miRNA rescue experiments were used to confirm the hsa_circ_0006646 –related regulatory axis in GC. Cell Counting Kit-8 (CCK-8), colony formation, wound healing, and Transwell experiments were performed to determine the effect of the hsa_ circ_0006646 –related regulatory axis on GC cells’ malignant behaviors in vitro . The xenograft tumor mouse model was established to evaluate the effect of hsa_circ_0006646 in vivo . Results hsa_circ_0006646 exhibited a high expression in GC tissues as compared to corresponding adjacent normal gastric mucosal epithelial tissues and its high expression was positively correlated with TNM stage, lymph node invasion and poor prognosis (P<0.05). Knockdown of hsa_circ_0006646 suppressed the proliferation, colony formation, migration, and invasion in GC cells (all P<0.05). hsa_circ_0006646 upregulated high mobility group box 1 ( HMGB1 ) by sponging miR-665 in GC cells (P<0.05). The hsa_circ_0006646 – miR-665–HMGB1 axis promoted malignant behaviors and epithelial–mesenchymal transition (EMT) in GC cells by activating the Wnt/β-catenin pathway (P<0.05). The existence of hsa_circ_0006646 – miR-665–HMGB1 axis was confirmed in GC specimens (P<0.05). Consequently, down-regulated hsa_circ_0006646 inhibited the progression and EMT of GC cells in vivo (P<...

show abstract

MicroRNA‑665 regulates the proliferation, apoptosis and adhesion of gastric cancer cells by binding to cadherin 3

Cited by 3 publications

References 27 publications

P-Cadherin Regulates Intestinal Epithelial Cell Migration and Mucosal Repair, but Is Dispensable for Colitis Associated Colon Cancer

P-Cadherin Regulates Intestinal Epithelial Cell Migration and Mucosal Repair, but Is Dispensable for Colitis Associated Colon Cancer

A novel circular RNA, circMAML3, promotes tumor progression of prostate cancer by regulating miR-665/MAPK8IP2 axis

Function of hsa_circ_0006646 as a competing endogenous RNA to promote progression in gastric cancer by regulating the miR-665–HMGB1 axis

Contact Info

Product

Resources

About