MAP30 promotes apoptosis of U251 and U87 cells by suppressing the LGR5 and Wnt/β-catenin signaling pathway, and enhancing Smac expression

Jiang, Yilin; Miao, Junjie; Wang, Dongliang; Zhou, Jingru; Liu, Bo; Jiao, Feng; Liang, Jian Feng; Wang, Yangshuo; Fan, Cungang; Zhang, Qingjun

doi:10.3892/ol.2018.8073

Cited by 13 publications

(9 citation statements)

References 47 publications

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“…Farago et al (36) demonstrated that following inhibition of Gsk-3β activity, the Wnt pathway is activated to promote breast cancer cell proliferation. Jiang et al (37) demonstrated that the expression levels of pGsk-3β Ser9 are increased in lung cancer tissues, and that the expression levels of pGsk-3β Ser9 are negatively correlated with lung cancer prognosis. Gsk-3β is a key kinase that determines the phosphorylation of β-catenin.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effects of miR‑26b‑5p on thyroid cancer

et al. 2019

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In order to examine the inhibitory effects of microRNA (miR)-26b-5p on thyroid cancer (TC), the clinicopathological features and pathological tissues of 67 patients were collected. The expression levels of miR-26b-5p were detected in TC and paracarcinoma tissues by quantitative polymerase chain reaction, and the association between miR-26b-5p expression and the clinicopathological features of the patients was analyzed using t-test or one-way analysis of variance. In addition, B-CPAP TC cells were infected with a lentivirus to induce miR-26b-5p overexpression and proliferation was detected by Cell Counting kit-8. Subsequently, migration and invasion were detected by Transwell and Matrigel assays, respectively, and the molecular mechanism of action was investigated by western blotting. The results demonstrated that the expression levels of miR-26b-5p were significantly lower in TC tissues compared with paracarcinoma tissues (P<0.01), and miR-26b-5p was associated with lymph node metastasis (P<0.05). In addition, overexpression of miR-26b-5p inhibited the proliferation, invasion and migration of B-CPAP cells. Western blot analysis demonstrated that the protein expression levels of phosphorylated glycogen synthase kinase-3β (pGsk-3β) were decreased, and the expression of β-catenin was decreased in B-CPAP cells overexpressing miR-26b-5p. These results demonstrated that miR-26b-5p may exert antitumor activity. In addition, at the molecular level, these effects may be associated with the Gsk-3β/β-catenin pathway.

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Section: Discussionmentioning

confidence: 99%

Inhibitory effects of miR‑26b‑5p on thyroid cancer

et al. 2019

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“…The extract inhibited proliferation and induced apoptosis in human and mouse adrenocortical cancer cells, whereas extract from blueberry, zucchini, and acorn squash did not show any cytotoxic effect [45]. MAP30 inhibited cell proliferation, migration and invasion and induced apoptosis in the glioma cell lines U87 and U251 in a time-and dose-dependent manner [23]. The methanol extract of fruit inhibited cell proliferation and increased cisplatin sensitivity in the ovarian cancer cell lines A2780cp, A2780s, C13* and OV2008 [54].…”

Section: Other Cancersmentioning

confidence: 91%

“…Similarly, methanol extract of fruit inhibited sphere formation and expression of CSC marker DCLK1 and Lgr5 in colon cancer cells [34]. MAP30 reduced expression of the self-renewal Wnt pathway effector molecule β-Catenin and its target genes c-Myc and cyclin D1 in glioma and prostate cancer cells [23,62]. Thus, bitter melon may have potential therapeutic implications against different cancers through its action on CSCs.…”

Section: Inhibition Of the Cancer Stem Cell Populationmentioning

confidence: 97%

Bitter Melon (Momordica Charantia), a Nutraceutical Approach for Cancer Prevention and Therapy

Sur

Ray

2020

Cancers

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Cancer is the second leading cause of death worldwide. Many dietary plant products show promising anticancer effects. Bitter melon or bitter gourd (Momordica charantia) is a nutrient-rich medicinal plant cultivated in tropical and subtropical regions of many countries. Traditionally, bitter melon is used as a folk medicine and contains many bioactive components including triterpenoids, triterpene glycoside, phenolic acids, flavonoids, lectins, sterols and proteins that show potential anticancer activity without significant side effects. The preventive and therapeutic effects of crude extract or isolated components are studied in cell line-based models and animal models of multiple types of cancer. In the present review, we summarize recent progress in testing the cancer preventive and therapeutic activity of bitter melon with a focus on underlying molecular mechanisms. The crude extract and its components prevent many types of cancers by enhancing reactive oxygen species generation; inhibiting cancer cell cycle, cell signaling, cancer stem cells, glucose and lipid metabolism, invasion, metastasis, hypoxia, and angiogenesis; inducing apoptosis and autophagy cell death, and enhancing the immune defense. Thus, bitter melon may serve as a promising cancer preventive and therapeutic agent.

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“…Cell Culture. U87 and HS683 cells are the most representative glioma cell lines [25,26] and are very sensitive to chidamide; therefore, they have been chosen in the present work. U87 and HS683 glioma cell lines were purchased from Cell Bank (Shanghai, China).…”

Section: Methodsmentioning

confidence: 99%

Chidamide Inhibits Glioma Cells by Increasing Oxidative Stress via the miRNA-338-5p Regulation of Hedgehog Signaling

Zhou

Liang

Wang³

et al. 2020

Oxidative Medicine and Cellular Longevity

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Objective. Chidamide has a broad spectrum of antitumor activity but its function on glioma remains unknown. The increase of reactive oxygen species (ROS) and reactive nitrogen species (RNS) may control glioma risk by promoting its apoptosis and necrosis. Hedgehog pathway is crucial to glioma cell proliferation and controls ROS production. We aimed to explore the effects of chidamide on the levels of miR-338-5p (glioma cell inhibitor), which may regulate Hedgehog signaling, resulting in the changes of RNS. Materials and Methods. Migration and invasion activities of glioma cells were measured by using the Transwell chamber assay. The expression levels of Sonic Hedgehog (Shh), Indian Hedgehog (Ihh), Desert Hedgehog (Dhh), miR-338-5p, and related molecules were detected by using real-time PCR (RT-PCR) and or Western Blot in U87 and HS683 glioma cells. The effects of chidamide on these molecules were measured by using the miR-338-5p inhibitor or mimics in U87 and HS683 glioma cell lines. ROS and RNS were measured by DCF DA and DAF-FM DA fluorescence. Biomarkers of oxidative stress were measured by using a corresponding kit. Apoptosis and necrosis rates were measured by using flow cytometry. Results. Chidamide inhibited the growth rate, migration, and invasion of human malignant glioma cells and increased the level of miR-338-5p. miR-338-5p inhibitor or mimics increased or inhibited the growth rate of U87 and HS683 glioma cells. Chidamide inhibited the levels of Shh, Ihh, migration protein E-cadherin, and invading protein MMP-2. The increase in the level of Shh and Ihh led to the reduction in the ROS and RNS levels. miR-338-5p inhibitor or mimics also showed a promoting or inhibitory function for the levels of Shh and Ihh. Furthermore, miR-338-5p mimics and inhibitor inhibited or promoted the migration and invasion of the glioma cells (P<0.05). Evaluated levels of miR-338-5p increased oxidative stress level and apoptosis and necrosis rate by regulating the levels of biomarkers of oxidative stress (P<0.05). Conclusion. Chidamide inhibits glioma cells by increasing oxidative stress via the miRNA-338-5p regulation of Hedgehog signaling. Chidamide may be a potential drug in the prevention of glioma development.

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MAP30 promotes apoptosis of U251 and U87 cells by suppressing the LGR5 and Wnt/β-catenin signaling pathway, and enhancing Smac expression

Cited by 13 publications

References 47 publications

Inhibitory effects of miR‑26b‑5p on thyroid cancer

Inhibitory effects of miR‑26b‑5p on thyroid cancer

Bitter Melon (Momordica Charantia), a Nutraceutical Approach for Cancer Prevention and Therapy

Chidamide Inhibits Glioma Cells by Increasing Oxidative Stress via the miRNA-338-5p Regulation of Hedgehog Signaling

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