MiR-324-5p reduces viability and induces apoptosis in gastric cancer cells through modulating TSPAN8

Lin, Hai; Zhou, Anni; Zhang, Jingyu; Liu, Shufang; Gu, J.-X.

doi:10.1111/jphp.12995

Cited by 31 publications

(23 citation statements)

References 21 publications

(44 reference statements)

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“…MiRNAs participate in diverse molecular and cellular processes, such as cellular migration/invasion, cell growth, apoptosis and signal transduction. MiRNAs dysregulation is a hallmark of many cancers, including glioblastoma, and they can be classified into tumour‐suppressive miRNAs and onco‐miRNAs . For example, miRNA‐744 expression is strongly repressed in glioblastoma, causing elevated transforming growth factor 1 beta (TGFB1) and dishevelled 2 (DVL2) expression and increased tumour cell migration .…”

Section: Introductionmentioning

confidence: 99%

“…MiRNAs dysregulation is a hallmark of many cancers, including glioblastoma, and they can be classified into tumour-suppressive miRNAs and onco-miRNAs. [24][25][26][27][28] For example, miRNA-744 expression is strongly repressed in glioblastoma, causing elevated transforming growth factor 1 beta (TGFB1) and dishevelled 2 (DVL2) expression and increased tumour cell migration. [29] In contrast, up-regulation of miRNA-21 in glioblastoma is associated with suppression of phosphatase and tensin homolog (PTEN), as well as programmed cell death 4 (PDCD4) expression, causing enhancement of cell survival and inhibition of apoptosis.…”

Section: Introductionmentioning

confidence: 99%

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MiRNA-7 enhances erlotinib sensitivity of glioblastoma cells by blocking the IRS-1 and IRS-2 expression

Alamdari-Palangi

Amini

Karami

2020

Journal of Pharmacy and Pharmacology

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Objectives Down‐regulation of miRNA‐7 is correlated with over‐expression of IRS‐1 and IRS‐2 proteins, the upstream regulators of IGF‐1R/Akt pathway, in glioblastoma cells. In this study, the effect of miRNA‐7 on expression of IRS‐1 and IRS‐2 and sensitivity of the U373‐MG glioblastoma cells to erlotinib was explored. Methods After miRNA‐7 transfection, the expression of IRS‐1 and IRS‐2 mRNAs was measured by RT‐qPCR. Trypan blue assay was used to assess the effect of miRNA‐7 on cell proliferation. The effects of miRNA‐7 and erlotinib, alone and in combination, on cell survival and apoptosis were measured using MTT assay and ELISA cell death assay, respectively. Key findings Our data showed that miRNA‐7 markedly inhibited the expression of IRS‐1 and IRS‐2 in a time‐dependent manner, inhibited the proliferation of glioblastoma cells and enhanced apoptosis (P < 0.05, relative to control). Pretreatment with miRNA‐7 synergistically inhibited the cell survival rate and decreased the IC50 of erlotinib. Furthermore, miRNA‐7 significantly augmented the apoptotic effect of erlotinib. Conclusions Our data propose that inhibition of IRS‐1 and IRS‐2 by miRNA‐7 can effectively induce apoptosis and sensitize glioblastoma cell to EGFR‐TKIs. Therefore, miRNA‐7 may be a potential therapeutic target in patients with glioblastoma.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MiRNA-7 enhances erlotinib sensitivity of glioblastoma cells by blocking the IRS-1 and IRS-2 expression

Alamdari-Palangi

Amini

Karami

2020

Journal of Pharmacy and Pharmacology

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“…In addition to KLF3, miR-324-5p is also reported to regulate the expression of CUEDC2, 21 ELAVL1, 25 ETS1, 26 EZH2, 39 GLI1, 27 HMGXB3, 40 PKM2, 41 SCF β-TrCP E3 ligase, 42 SP1, 26 TSPAN8, 43 and WASF-2, 40 in turn eliciting downstream effects associated with these genes. KLF3 is an important regulator for the biological processes, including adipogenesis, erythropoiesis, and B cell development.…”

Section: Discussionmentioning

confidence: 99%

miR-324-5p Contributes to Cell Proliferation and Apoptosis in Pancreatic Cancer by Targeting KLF3

Wan

Luo

Yang

et al. 2020

Molecular Therapy - Oncolytics

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Pancreatic cancer cells are characterized by high cell proliferation and low cell apoptosis, but the factors involved in these processes remain to be further studied. In this study, we report that miR-324-5p regulates the proliferation and apoptosis of pancreatic cancer cells through regulating the expression of Krüppel-like factor 3 (KLF3). In both pancreatic cancer tissues and cell lines, the levels of miR-324-5p are significantly increased. Inhibition of miR-324-5p represses cell proliferation but promotes cell apoptosis, whereas overexpression of miR-324-5p exerts the opposite effect. Furthermore, we identified KLF3, a factor regulating pancreatic cancer cell proliferation and apoptosis, as a new direct downstream target of miR-324-5p. Our results suggest that miR-324-5p plays an important role in pancreatic cancer cell proliferation and apoptosis via downregulating the expression of KLF3.

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“…Studies have shown that miR-324-5p can inhibit gallbladder carcinoma cell metastasis by downregulating the expression level of transforming growth factor β2 ( TGFB2 ), 19 as well as suppress the migration and induce the apoptosis of gastric cancer cells by inhibiting TSPAN8 . 20 Another study found that miR-324-5p can promote the osteogenic differentiation of human mesenchymal stem cells (MSCs) and murine C3H10T1/2 cells by regulating the Hedgehog signaling pathway. 21 Mesenchymal stem cells have the potential for myogenic differentiation, 22 indicating that miR-324-5p has a potential role in myogenic differentiation.…”

Section: Introductionmentioning

confidence: 99%

miR-324-5p Inhibits C2C12 cell Differentiation and Promotes Intramuscular Lipid Deposition through lncDUM and PM20D1

Liu

Wang

Zhou

et al. 2020

Molecular Therapy - Nucleic Acids

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Skeletal muscle is an important metabolic organ of the body, and impaired skeletal muscle differentiation can result in a wide range of metabolic diseases. It has been shown that microRNAs (miRNAs) play an important role in skeletal muscle differentiation. The aim of this study was to investigate the role of mmu-miR-324-5p in the differentiation of C2C12 myoblasts and lipid droplet deposition in myotubes for future targeted therapies. We found that mmu-miR-324-5p was highly expressed in mouse skeletal muscle. Overexpression of miR-324-5p significantly inhibited C2C12 myoblast differentiation while promoting oleate-induced lipid accumulation and β-oxidation in C2C12 myoblasts. Conversely, inhibition of mmu-miR-324-5p promoted C2C12 myoblast differentiation and inhibited lipid deposition in myotubes. Mechanistically, mmu-miR-324-5p negatively regulated the expression of long non-coding Dum (lncDum) and peptidase M20 domain containing 1 (Pm20d1) in C2C12 myoblasts. Reduced lncDum expression was associated with a significant decrease in the expression of myogenesis-related genes. Knockdown of mmu-miR-324-5p increased the levels of lncDum and myogenesis-related gene expression. Following oleate-induced lipid deposition in C2C12 myoblasts, overexpression of mmu-miR-324-5p decreased the expression of Pm20d1 while increasing the expression of mitochondrial β-oxidation and long-chain fatty acid synthesis-related genes. In conclusion, we provide evidence that miR-324-5p inhibits C2C12 myoblast differentiation and promotes intramuscular lipid deposition by targeting lncDum and Pm20d1, respectively.

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MiR-324-5p reduces viability and induces apoptosis in gastric cancer cells through modulating TSPAN8

Abstract: This study suggested a novel, probable mechanism of miR-324-5p in gastric cancer context and revealed that miR-324-5p inhibited gastric cancer cell survival by targeting TSPAN8.

Cited by 31 publications

References 21 publications

MiRNA-7 enhances erlotinib sensitivity of glioblastoma cells by blocking the IRS-1 and IRS-2 expression

MiRNA-7 enhances erlotinib sensitivity of glioblastoma cells by blocking the IRS-1 and IRS-2 expression

miR-324-5p Contributes to Cell Proliferation and Apoptosis in Pancreatic Cancer by Targeting KLF3

miR-324-5p Inhibits C2C12 cell Differentiation and Promotes Intramuscular Lipid Deposition through lncDUM and PM20D1

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