PTEN inhibits the migration and invasion of HepG2 cells by coordinately decreasing MMP expression via the PI3K/Akt pathway

Tian, Tao; Kang, Nan; Guo, Hui; Wang, Wen‐Juan; Ruan, Zhiping; Wang, Shuhong; Liu, Xuan; Lu, Chuang-Xin

doi:10.3892/or_00000800

Cited by 24 publications

(4 citation statements)

References 31 publications

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“…HCC cells proliferate, invade, and metastasize through a variety of signaling pathways during tumor progression. 19 In the current study, we uncovered that HZC could promote the activation of the p38 MAPK pathway, then potentiating apoptosis of HepG2 cells and ultimately retarding the progression of HCC.…”

Section: Discussionmentioning

confidence: 72%

Hydrazinocurcumin Induces Apoptosis of Hepatocellular Carcinoma Cells Through the p38 MAPK Pathway

Qiao

Wang

et al. 2020

Clinical Translational Sci

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Hydrazinocurcumin (HZC), a synthetic derivative of curcumin (CUR), has been documented to show anticancer potential in impeding tumor growth in several cancers, including hepatocellular carcinoma (HCC). However, the underlying molecular mechanisms remain unclear. This study aimed to explore the function and underlying mechanisms of HZC on HCC cells, which may involve the p38 mitogen activated protein kinase (MAPK) pathway. HZC was first purified and identified. HepG2 cells were then subjected to treatment with HZC or CUR of different concentrations and p38 MAPK signaling inhibitor (SB203580) to verify their effects on HCC cell apoptosis and proliferation. Furthermore, the functional relevance between HZC and the p38 MAPK pathway in HCC was examined. It was observed that 40 μM HZC exhibited the best pro-apoptosis effect in HCC cells. HZC was found to inhibit HCC cell proliferation and promote apoptosis, the effect of which was stronger than 5-fluorouracil (5-FU). More importantly, the anti-oncogenic effect of HZC and 5-FU was implicated with activation of the p38 MAPK pathway. In vivo experimental results showed that HZC inhibited tumor growth more effectively than 5-FU through the p38 MAPK pathway. These results provide evidence that HZC exerted anti-oncogenic and pro-apoptosis effects in HCC cells through activation of the p38 MAPK pathway.

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Section: Discussionmentioning

confidence: 72%

Hydrazinocurcumin Induces Apoptosis of Hepatocellular Carcinoma Cells Through the p38 MAPK Pathway

Qiao

Wang

et al. 2020

Clinical Translational Sci

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“…Effects of flaccidoxide on the PI3K/AKT/mTOR/p70S6K pathway in BFTC-905 and T24 bladder cancer cells. Tian et al (31) showed that the PI3K/AKT/mTOR pathway is involved in cell proliferation, differentiation, survival and apoptosis. Therefore, we next investigated whether inhibition of the PI3K/AKT/mTOR pathway occurs in cells treated with flaccidoxide, which then prevents bladder cancer cell growth by triggering apoptosis.…”

Section: Resultsmentioning

confidence: 99%

Flaccidoxide Induces Apoptosis Through Down-regulation of PI3K/AKT/mTOR/p70S6K Signaling in Human Bladder Cancer Cells

Wong

et al. 2021

Anticancer Res

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Background/Aim: Urothelial carcinoma (UC) is the most common type of genitourinary cancer with high incidence and mortality rates in men. In this study, we used the BFTC-905 and T24 bladder cancer cell lines as in vitro models to investigate the pathways involved in flaccidoxideinduced apoptosis. Materials and Methods: We utilized MTT assays, colony assays, wound-healing assays and fluorescence with TUNEL to confirm the cytotoxicity of flaccidoxide in bladder cancer cell lines. Potential proliferative and apoptotic molecular mechanisms were evaluated by western blotting. Results: The expression of anti-apoptotic proteins Bcl-2 and phosphorylated Bad (p-Bad) was attenuated with an increasing flaccidoxide concentration, while the expression of proapoptotic proteins Bax, Bad, cleaved caspase-3, cleaved caspase-9 and cleaved PARP-1 was found increased. Additionally, phosphorylation of phosphoinositide 3-kinases (PI3K), protein kinase B (AKT) and mammalian target of rapamycin (mTOR) in the PI3K/AKT/mTOR pathway was reduced, leading to a reduction in the phosphorylation of downstream 70-kDa ribosomal protein S6 kinase 1 (p70S6K), S6 ribosomal protein (S6) and eukaryotic translation initiation factor 4B (eIF4B). However, eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) protein phosphorylation was increased due to attenuation of the upstream phosphorylation of mTOR protein. Conclusion: Flaccidoxide-induced apoptosis in BFTC-905 and T24 cells is mediated by mitochondrial dysfunction and down-regulation the PI3K/AKT/mTOR/p70S6K signaling pathway.

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“…13 A study showed that PTEN, as a crucial tumor suppressor, suppresses HepG2 cells growth, migration, and invasion in a PI3K/AKT-dependent manner. 31 The blockage of PTEN/PI3K/AKT was indicative of an antitumor effect of SEVO in Huh7 and HepG2 cells. Consequently, Dnmt3a silence emerged as a central mediator for the antitumor property.…”

Section: Discussionmentioning

confidence: 99%

“…Dnmt3a silences PTEN via DNA methylation . A study showed that PTEN, as a crucial tumor suppressor, suppresses HepG2 cells growth, migration, and invasion in a PI3K/AKT‐dependent manner . The blockage of PTEN/PI3K/AKT was indicative of an antitumor effect of SEVO in Huh7 and HepG2 cells.…”

Section: Discussionmentioning

confidence: 99%

Antitumor activity of sevoflurane in HCC cell line is mediated by miR‐29a‐induced suppression of Dnmt3a

Guang-ming

Tian

Cheng

et al. 2019

J of Cellular Biochemistry

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Sevoflurane (SEVO) is widely applied as an anesthetic. More recently, its antitumor capacity has been reported. However, potent mechanisms are still incompletely ascertained. In our current study, we attempted to elucidate a potent mechanism associated with microRNA (miR)‐29a/DNA methyltransferase 3 alpha (Dnmt3a) in hepatocellular carcinoma (HCC) cells. After transfection and stimulation with SEVO, biological activities of Huh7 and HepG2 cells were evaluated using the cell counting kit‐8, Annexin V‐fluorescein isothiocyanate apoptosis detection kit, 24‐well cell migration assay kit, and tumor invasion 24‐well plates. miR‐29a and protein expression were quantified with quantitative reverse transcription polymerase chain reaction and Western blot assay, respectively. A Dual‐Luciferase Reporter Assay System was used to verify whether miR‐29a targets Dnmt3a. We found that SEVO alleviated cell viability, aggrandized apoptosis, and impeded migration and invasion of the Huh7 and HepG2 cells. Besides, SEVO enhanced phosphatase and tensin homolog (PTEN) expression, and phosphorylated expression of phosphatidylinositol 3 kinase (PI3K), and protein kinase B (AKT) was eliminated by SEVO. Of note, SEVO restored miR‐29a which was downregulated in HCC tissues and cells. miR‐29a inhibitor abolished the positive effects of SEVO on the biological processes. Dual‐Luciferase Reporter assay showed miR‐29a repressed Dnmt3a expression via targeting its 3′‐untranslated region. Further, exogenous expression of Dnmt3a partially repressed PTEN and enhanced phosphorylated expression of PI3K and AKT which were originally elevated or diminished by SEVO. In conclusion, SEVO restored the expression of miR‐29a, which posttranscriptionally downregulated Dnmt3a, and then exhibited an antitumor property in HCC cells.

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PTEN inhibits the migration and invasion of HepG2 cells by coordinately decreasing MMP expression via the PI3K/Akt pathway

Cited by 24 publications

References 31 publications

Hydrazinocurcumin Induces Apoptosis of Hepatocellular Carcinoma Cells Through the p38 MAPK Pathway

Hydrazinocurcumin Induces Apoptosis of Hepatocellular Carcinoma Cells Through the p38 MAPK Pathway

Flaccidoxide Induces Apoptosis Through Down-regulation of PI3K/AKT/mTOR/p70S6K Signaling in Human Bladder Cancer Cells

Antitumor activity of sevoflurane in HCC cell line is mediated by miR‐29a‐induced suppression of Dnmt3a

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