MicroRNA‐3191 promotes migration and invasion by downregulating TGFBR2 in colorectal cancer

He, Hongbin; Zhao, Xiaojuan; Zhu, Zijue; Du, Le; Chen, Erfei; Liu, Shuzhen; Dong, Jing; Yang, Jin

doi:10.1002/jbt.22308

Cited by 22 publications

(14 citation statements)

References 25 publications

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“…In addition, bioinformatics analysis predicted TGFBR2 as a potential target gene of miR-23a-3p. Despite little emphasis on TGFBR2 in the literature, its mutation and downregulation was detected in various types of cancer such as colorectal cancer, lung cancer and breast cancer (20,(29)(30)(31)(32). Furthermore, Shima et al (33) reported that mutations in TGFBR2 were associated with 5-year survival rates in colorectal cancer.…”

Section: Discussionmentioning

confidence: 99%

Insight into the effects of microRNA‑23a‑3p on pancreatic cancer and its underlying molecular mechanism

et al. 2019

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Previous studies have demonstrated that microRNA (miR)-23a-3p plays a role as an oncogene that is involved in several different types of carcinoma. However, few studies investigated the association between miR-23a-3p and pancreatic cancer (PC). The aim of the present study was to elucidate the biological functions of miR-23a-3p in PC and to investigate its underlying molecular mechanisms. The expression of miR-23a-3p in PC and adjacent normal tissues was investigated using microarrays. In order to validate the outcomes of the microarray results, reverse transcription-quantitative (RT-q)PCR was used to determine the expression levels of miR-23a-3p in PC tissues and cell lines. Furthermore, functional analyses were conducted following miR-23a-3p inhibition and overexpression, in order to assess the proliferation, invasion and migration of PC cells. Bioinformatics analysis indicated transforming growth factor-β receptor type II (TGFBR2) as a potential direct target of miR-23a-3p. Western blotting was performed in order to determine the protein expression of TGFBR2 in PC cell lines. The findings from the microarray demonstrated upregulation of miR-23a-3p in PC compared with normal tissues. RT-qPCR revealed significantly higher levels of miR-23a-3p expression in PC compared with normal control tissues or cells. Furthermore, miR-23a-3p was demonstrated to promote the proliferation, invasion and migration of PC cells, which was suppressed by the inhibition of miR-23a-3p. In addition, the miR-23a-3p expression level was negatively associated with TGFBR2 expression. Overall, the present study demonstrated the tumor-promoting effects of miR-23a-3p in PC cells. Furthermore, miR-23a-3p is a potential oncogenic regulator of PC, by targeting TGFBR2, and a biomarker or target for molecular therapy.

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Section: Discussionmentioning

confidence: 99%

Insight into the effects of microRNA‑23a‑3p on pancreatic cancer and its underlying molecular mechanism

et al. 2019

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“…Cell migration ability was evaluated using a previously described wound healing assay (20). After growing the 16HBE cells to 90% confluence in six-well plates, the cell layers were horizontally scraped using a sterile 10 mL pipette tip across the plate.…”

Section: Wound Healing Assaymentioning

confidence: 99%

Sinomenine Relieves Airway Remodeling By Inhibiting Epithelial-Mesenchymal Transition Through Downregulating TGF-β1 and Smad3 Expression In Vitro and In Vivo

Cao

Wang

et al. 2021

Front. Immunol.

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Airway remodeling is associated with dysregulation of epithelial-mesenchymal transition (EMT) in patients with asthma. Sinomenine (Sin) is an effective, biologically active alkaloid that has been reported to suppress airway remodeling in mice with asthma. However, the molecular mechanisms behind this effect remain unclear. We aimed to explore the potential relationship between Sin and EMT in respiratory epithelial cells in vitro and in vivo. First, 16HBE cells were exposed to 100 μg/mL LPS and treated with 200 μg/mL Sin. Cell proliferation, migration, and wound healing assays were performed to evaluate EMT, and EMT-related markers were detected using Western blotting. Mice with OVA-induced asthma were administered 35 mg/kg or 75 mg/kg Sin. Airway inflammation and remodeling detection experiments were performed, and EMT-related factors and proteins in the TGF-β1 pathway were detected using IHC and Western blotting. We found that Sin suppressed cell migration but not proliferation in LPS-exposed 16HBE cells. Sin also inhibited MMP7, MMP9, and vimentin expression in 16HBE cells and respiratory epithelial cells from mice with asthma. Furthermore, it decreased OVA-specific IgE and IL-4 levels in serum, relieved airway remodeling, attenuated subepithelial collagen deposition, and downregulating TGF-β1and Smad3 expression in mice with asthma. Our results suggest that Sin suppresses EMT by inhibiting IL-4 and downregulating TGF-β1 and Smad3 expression.

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“…mirnas are rna molecules 21-23 nucleotides in length, which do not encode proteins but regulate gene expression through binding to specific miRNA-binding sites on target mrnas (14,15). mirnas act as biological regulators in a range of cellular processes, such as cell proliferation, invasion and apoptosis or programmed cell death (16,17). notably, mir-374a negatively regulates its downstream genes to control the proliferation and invasion of cancer cells (18).…”

Section: Introductionmentioning

confidence: 99%

Propofol inhibits proliferation and cisplatin resistance in ovarian cancer cells through regulating the microRNA‑374a/forkhead box O1 signaling axis

Sun

Peng

et al. 2020

Mol Med Report

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ovarian cancer is a prominent disease that demonstrates high incidence rates in women and often presents multidrug resistance. Propofol has been demonstrated to suppress the malignancy of various types of human cancer; however, the underlying molecular mechanisms of propofol in ovarian cancer remain largely unknown. The present study aimed to investigate whether and how propofol inhibits proliferation and cisplatin (ddP) resistance in ovarian cancer cells. ovarian cancer cell viability was assessed by the cell counting kit-8 assay; apoptosis and cell cycle progression were determined by flow cytometry; the relative expression levels of microRNA (miR)-374a and forkhead box O1 (FOXO1) were analyzed using reverse transcription-quantitative Pcr; the binding ability of miR-374a to FOXO1 was assessed by the dual-luciferase reporter assay; cellular sensitivity to ddP was detected using the MTT assay; and finally, the protein expression levels of FOXO1, p27, and Bcl-2-like-protein 11 (Bim) were analyzed by western blotting. Propofol reduced viability, promoted apoptosis and decreased mir-374a expression levels in A2780 cells. In addition, the viability of a2780/ddP cells in the propofol + ddP treatment group was significantly inhibited, and the apoptotic rate was increased. In addition, miR-374a overexpression increased cell viability and the proportion of cells in the S phase, and decreased the proportion of cells in the G0/G1 phase. conversely, genetic knockdown of miR-374a exerted the opposite effects on cell viability and cell cycle progression. Moreover, mir-374a was demonstrated to bind to FOXO1. Propofol promoted the expression of FOXO1, p27 and Bim, induced cell cycle arrest and decreased ovarian cancer cell viability. in addition, treatment with propofol and DDP regulated FOXO1 and increased apoptosis of ovarian cancer cells. in conclusion, propofol downregulated mir-374a and modulated the FOXO1 pathway to reduce proliferation and DDP resistance in ovarian cancer cells.

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MicroRNA‐3191 promotes migration and invasion by downregulating TGFBR2 in colorectal cancer

Cited by 22 publications

References 25 publications

Insight into the effects of microRNA‑23a‑3p on pancreatic cancer and its underlying molecular mechanism

Insight into the effects of microRNA‑23a‑3p on pancreatic cancer and its underlying molecular mechanism

Sinomenine Relieves Airway Remodeling By Inhibiting Epithelial-Mesenchymal Transition Through Downregulating TGF-β1 and Smad3 Expression In Vitro and In Vivo

Propofol inhibits proliferation and cisplatin resistance in ovarian cancer cells through regulating the microRNA‑374a/forkhead box O1 signaling axis

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