MiR-132 inhibits migration and invasion and increases chemosensitivity of cisplatin-resistant oral squamous cell carcinoma cells via targeting TGF-β1

Chen, Liqiang; Zhu, Qingli; Lu, Lingwei; Liu, Yanshan

doi:10.1080/21655979.2019.1710925

Cited by 55 publications

(43 citation statements)

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“…MicroRNAs (miRNAs) are a class of short noncoding RNAs that have emerged as significant epigenetic regulators of cellular functions, predominantly through silencing of their target genes via direct complementary mRNA 3′UTR base pairing [10]. Dysregulation of miRNAs has been reported in numerous cancers where individual miRNAs behave in an oncogenic or tumor suppressor manner [11][12][13][14]. To date, several profiling studies have reported that miRNAs are associated with clinical outcome in NB [15] and specific miRNAs have been identified to regulate key processes such as apoptosis, differentiation, cell proliferation and cell invasiveness in NB [16][17][18].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-145 overexpression inhibits neuroblastoma tumorigenesis in vitro and in vivo

Zhao

Zhou

et al. 2020

Bioengineered

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Neuroblastoma (NB) is responsible for 15% of all childhood cancer deaths. Despite advances in treatment and disease management, the overall 5-year survival rates remain poor in high-risk disease (25-40%). It is well known that miR-145 functions as a tumor suppressor in several types of cancer. However, the impact of miR-145 on NB is still ambiguous. Our aim was to investigate the potential tumor suppressive role and mechanisms of miR-145 in high-risk neuroblastoma. Expression levels of miR-145 in tissues and cells were determined using RT-qPCR. The effect of miR-145 on cell viability was evaluated using MTT assays, apoptosis levels were determined using TUNEL staining, and the MTDH protein expression was determined using western blot and RT-PCR. Luciferase reporter plasmids were constructed to confirm direct targeting for MTDH. The results showed that miR-145 expression was significantly lower in high-risk MYCN amplified (MNA) tumors and low miR-145 expression was associated with worse EFS and OS in our cohort. Over-expression of miR-145 reduced cell viability and increased apoptosis in SH-SY-5Y cells. We identified MTDH as a direct target for miR-145 in SH-SY-5Y cells. Targeting MTDH has the similar results as miR-145 overexpression. Our findings suggest that low miR-145 expression was associated with poor prognosis in patients with NB, and the overexpression of miR-145 inhibited NB cells growth by down-regulating MTDH, thus providing a potential target for the development of microRNA-based approach for NB therapy.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-145 overexpression inhibits neuroblastoma tumorigenesis in vitro and in vivo

Zhao

Zhou

et al. 2020

Bioengineered

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“…Several other studies have revealed that miRNAs may serve as biomarkers of CRC, and the majority of these miRNAs have a tumor suppressor role ( 27 , 28 ). miR-132 has been demonstrated to regulate cancer via regulation of several cellular behaviors, including tumorigenesis, proliferation, resistance and progression ( 29 ). Previous studies have indicated that miR-132 exerts tumor-suppressing functions in various types of cancer, including prostate cancer, thyroid cancer, pancreatic cancer, cervical cancer and renal carcinoma ( 30 – 35 ).…”

Section: Discussionmentioning

confidence: 99%

Halofuginone inhibits tumorigenic progression of 5‑FU‑resistant human colorectal cancer HCT‑15/FU cells by targeting miR‑132‑3p <em>in vitro</em>

Wang¹,

Zhu²,

Yan

et al. 2020

Oncol Lett

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5-Fluorouracil (5-FU)-based chemotherapy is the first-line option for patients with advanced colorectal cancer (CRC). However, the development of chemoresistance is the primary cause of treatment failure. Halofuginone (HF), a small molecule alkaloid derived from febrifugine, has been demonstrated to exert strong anti-proliferative effects. However, to the best of our knowledge, whether HF inhibits the progression of 5-FU-resistant human CRC HCT-15/FU cells, and the underlying mechanisms, remain unknown. In the present study, the effects of HF on HCT-15/FU cells were assessed in vitro . The results revealed that HF inhibited HCT-15/FU cell viability as demonstrated by the MTT and colony formation assays. Following treatment of HCT-15/FU cells with HF, the migratory and invasive capacities of the cells were significantly decreased. MicroRNA (miRNA/miR)-sequencing data, subsequent miRNA trend analysis and reverse transcription-quantitative PCR all demonstrated that miR-132-3p expression was increased following treatment with HF in a dose-dependent manner. Western blot analysis indicated that following treatment with HF, the expression levels of proteins associated with proliferation, invasion and metastasis in cells were markedly downregulated. These results suggested that HF inhibited the proliferation, invasion and migration of HCT-15/FU cells by upregulating the expression levels of miR-132-3p. Therefore, miR-132-3p may serve as a molecular marker, which may be used to predict CRC resistance to 5-FU, and HF may serve as a novel clinical treatment for 5-FU-resistant CRC.

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“…TGF-β1 has extensive biological functions, including regulating cell growth, differentiation, migration, matrix formation, and damage repair [24][25][26]. It is the most in-depth and most powerful pro brotic cytokine currently studied [27][28][29].…”

Section: Discussionmentioning

confidence: 99%

Mycophenolate mofetil reduces epidural fibrosis by regulating TGF-β1/Smad2/3 axis to repress the proliferation, migration and differentiation of fibroblasts

Zhu¹,

Zhang²,

Zhang³

et al. 2020

Preprint

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Background Excessive fibroblasts proliferation is believed as a major reason in the process of epidural fibrosis, which is known as a troublesome complication of lumbar laminectomy clinically. Mycophenolate mofetil (MMF) is a kind of immunosuppressant, previous studies had shown that it has the function of preventing fibrosis, but the role and mechanism are still unclear. In this study, we determined the repressed effect of MMF on fibroblasts proliferation, migration and differentiation in surgical-induced epidural fibrosis and the underlying mechanism. Methods In vitro, the impacts of MMF on cell viability were measured by cell counting kit-8 (CCK-8) assay and the fibroblasts proliferation rates were determined by using EdU incorporation, cell cycle assays and western blot. Additionally, the impacts of MMF on fibroblasts migration and differentiation were analyzed by cell wound scratch assay, transwell assay, immunofluorescence analysis and western blot. In vivo, we built epidural fibrosis models in rats and locally applied MMF. Histological and immunohistochemical staining were used to determine the effect of MMF on reducing epidural fibrosis and fibroblasts functions. Results CCK-8 assay demonstrated that MMF repressed fibroblasts proliferation in a time- and a dose-dependent manner. EdU incorporation assay and cell cycle analysis proved the inhibition effect of MMF on the proliferation of fibroblasts. Cell wound scratch assay, transwell assay and immunofluorescence proved the inhibition effect of MMF on the migration and differentiation of fibroblasts. Western blotting analysis proved that MMF inhibited the expression of TGF-β1, p-Smad2 and p-Smad3. The expression of proliferation proteins, migration proteins and differentiation proteins were downregulated. In addition, histological and immunohistochemical stain showed that MMF reduces epidural fibrosis by repressing the proliferation, migration and differentiation of fibroblasts. Conclusion MMF could inhibit the proliferation, migration and differentiation of fibroblasts, it reduced surgical-induced epidural fibrosis as well. TGF-β1/Smad2/3 axis may be the latent mechanism in MMF reduced epidural fibrosis. It might provide a new notion for mitigating surgery-induced epidural fibrosis.

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MiR-132 inhibits migration and invasion and increases chemosensitivity of cisplatin-resistant oral squamous cell carcinoma cells via targeting TGF-β1

Abstract: View related articles View Crossmark data Citing articles: 1 View citing articles RESEARCH PAPER MiR-132 inhibits migration and invasion and increases chemosensitivity of cisplatin-resistant oral squamous cell carcinoma cells via targeting TGF-β1

Cited by 55 publications

References 44 publications

MicroRNA-145 overexpression inhibits neuroblastoma tumorigenesis in vitro and in vivo

MicroRNA-145 overexpression inhibits neuroblastoma tumorigenesis in vitro and in vivo

Halofuginone inhibits tumorigenic progression of 5‑FU‑resistant human colorectal cancer HCT‑15/FU cells by targeting miR‑132‑3p <em>in vitro</em>

Mycophenolate mofetil reduces epidural fibrosis by regulating TGF-β1/Smad2/3 axis to repress the proliferation, migration and differentiation of fibroblasts

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MiR-132 inhibits migration and invasion and increases chemosensitivity of cisplatin-resistant oral squamous cell carcinoma cells via targeting TGF-β1

Abstract: View related articles View Crossmark data Citing articles: 1 View citing articles RESEARCH PAPER MiR-132 inhibits migration and invasion and increases chemosensitivity of cisplatin-resistant oral squamous cell carcinoma cells via targeting TGF-β1

Cited by 55 publications

References 44 publications

MicroRNA-145 overexpression inhibits neuroblastoma tumorigenesis in vitro and in vivo

MicroRNA-145 overexpression inhibits neuroblastoma tumorigenesis in vitro and in vivo

Halofuginone inhibits tumorigenic progression of 5‑FU‑resistant human colorectal cancer HCT‑15/FU cells by targeting miR‑132‑3p <em>in&nbsp;vitro</em>

Mycophenolate mofetil reduces epidural fibrosis by regulating TGF-β1/Smad2/3 axis to repress the proliferation, migration and differentiation of fibroblasts

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Halofuginone inhibits tumorigenic progression of 5‑FU‑resistant human colorectal cancer HCT‑15/FU cells by targeting miR‑132‑3p <em>in vitro</em>