Torilis japonica extract-generated intracellular ROS induces apoptosis by reducing the mitochondrial membrane potential via regulation of the AMPK-p38 MAPK signaling pathway in HCT116 colon cancer

Kim, Guen Tae; Lee, Se Hee; Kim, Young Min

doi:10.3892/ijo.2016.3578

Cited by 25 publications

(13 citation statements)

References 41 publications

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“…Among these is the mitogen activated protein kinase (MAPK) signaling pathway, which regulates the expression of a large number of proteins involved in the control of cell proliferation, differentiation and apoptosis (6,7), and remains a focus of investigation for therapeutic targeting, along with the development of appropriate inhibitors (8). These inhibitors have been demonstrated to be effective for the treatment of oral cancer and other malignancies, including human colon cancer, breast cancer and lung cancer (9)(10)(11)(12). Certain inhibitors, which have been examined in various clinical trials, are being used to treat patients with oral cancer and are eliciting promising results.…”

Section: Introductionmentioning

confidence: 99%

Mitogen-activated protein kinase signaling pathway in oral cancer (Review)

et al. 2017

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Abstract. The mitogen-activated protein kinase (MAPK) signaling pathway is associated with tumor cell proliferation, differentiation, apoptosis, angiogenesis, invasion and metastasis. The present review assesses the involvement of the MAPK signaling pathway in oral cancer progression and invasion based on analysis of individual sub-pathways and their mechanisms of action. The regulation of this pathway for targeted oral cancer therapy is explored and the challenges confronting this, as well as corresponding potential solutions, are discussed. Exploring this pathway with an emphasis on its components, subfamilies, sub-pathways, interactions with other pathways and clinical practice modes may improve oral cancer treatment.

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Section: Introductionmentioning

confidence: 99%

Mitogen-activated protein kinase signaling pathway in oral cancer (Review)

et al. 2017

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“…The balance of MMP is important for maintaining the normal function of mitochondria. Thus, decreased MMP triggers mitochondrial swelling and rupturing of outer membrane, ultimately leading to apoptosis of cells [20,21].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-182-5p protects human lens epithelial cells against oxidative stress-induced apoptosis by inhibiting NOX4 and p38 MAPK signalling

Yuan

2020

BMC Ophthalmol

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Background MicroRNAs (miRNAs) are abnormally expressed in various ocular diseases, including age-related cataract. However, the role of miR-182-5p in the progression of age-related cataract remains unclear. Methods The expression of miR-182-5p in HLE-B3 cells was detected by qRT-PCR. HLE-B3 cells were transfected with miR-182-5p mimics. CCK-8, EdU, flow cytometry, 2′,7′-dichlorodihydrofluorescein diacetate, JC-1 kit, and western blot were used to assess the cell viability, proliferation, apoptosis, reactive oxygen species (ROS) level, mitochondrial membrane potential (MMP), and protein expression, respectively, in vitro. The relationship between miR-182-5p and NOX4 was confirmed using the dual-luciferase reporter gene analysis. Results We found that miR-182-5p expression was significantly decreased by the H2O2 exposure. Overexpression of miR-182-5p promoted cell proliferation and inhibited ROS production and apoptosis in H2O2-induced HLE-B3 cells. Moreover, p-p-38, p-ERK, and p-JNK were up-regulated in H2O2-treated HLE-B3 cells, and overexpression of miR-182-5p reversed the effects of H2O2 on HLE-B3 cells. In addition, dual-luciferase reporter assay substantiated that NOX4 was a direct target and downregulated by miR-182-5p. Conclusions We concluded that miR-182-5p inhibited lens epithelial cells apoptosis through regulating NOX4 and p38 MAPK signaling, providing a novel biomarker for treatment of age-related cataract.

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“…Flupentixol, for instance, could be specifically docked to PI3K to inhibit the PI3K/AKT pathway and survival of lung cancer cells ( 27 ). Meanwhile, torilis japonica extract induced apoptosis by reducing the mitochondrial membrane potential via the regulation of the AMPK-p38 MAPK signaling pathway ( 28 ), and Paris Saponin I enhanced apoptosis by influencing the p38 MAPK, ERK, and Akt pathways in lung cancer cells ( 4 ). Both Akt and p38 MAPK are involved in a large number of antitumor activities, and sometimes, both are involved.…”

Section: Discussionmentioning

confidence: 99%

Plantamajoside modulates the proliferation, stemness, and apoptosis of lung carcinoma via restraining p38MAPK and AKT phosphorylation

Li¹,

Han²,

Cao³

2020

Transl Cancer Res TCR

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Background Plantamajoside (PMS), an active anti-inflammatory component and antioxidant derived from Herba Plantaginis , has been reported to exert a suppressive effect in liver cancer in vivo . In this study, we tested the effects of PMS on the metastatic 95D cell line. Methods 95D cells were characterized as most sensitive to PMS across several lung cancer cell lines. Cell viability within 24 h was tested with CCK-8. Different concentrations of PMS (0, 50, 100, and 200 µg/mL) and 5 µg/mL of cisplatin were established for later 24 h treatment. Relative mRNA and protein expression were assessed with PCR and Western blotting. Cell proliferation and stemness were indicated with colony and sphere formation. Cell metastasis was evaluated with wound healing and Transwell. Apoptotic cells and mitochondrial membrane potential were investigated with flow cytometry. Results CCK-8 assay showed PMS to inhibit the viability of 95D cells in a dose-dependent manner. PMS decreased colony formation and inhibited stemness in 95D cells. Invasion and migration were also inhibited. Moreover, PMS induced cell apoptosis, and decreased mitochondrial membrane potential. All of these effects were dose dependent. Interestingly, PMS treatment reduced the protein expression of p-p38 MAPK and p-AKT but not that of p38 MAPK and AKT. Conclusions PMS inhibited proliferation, stemness, and migration, and initiated apoptosis in 95D cells, possibly through p38 MAPK and AKT dephosphorylation and mitochondria dysfunction. These findings support the promise of PMS as a prodrug in lung cancer treatment.

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Torilis japonica extract-generated intracellular ROS induces apoptosis by reducing the mitochondrial membrane potential via regulation of the AMPK-p38 MAPK signaling pathway in HCT116 colon cancer

Cited by 25 publications

References 41 publications

Mitogen-activated protein kinase signaling pathway in oral cancer (Review)

Mitogen-activated protein kinase signaling pathway in oral cancer (Review)

MicroRNA-182-5p protects human lens epithelial cells against oxidative stress-induced apoptosis by inhibiting NOX4 and p38 MAPK signalling

Plantamajoside modulates the proliferation, stemness, and apoptosis of lung carcinoma via restraining p38MAPK and AKT phosphorylation

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