Wogonin Increases Cisplatin Sensitivity in Ovarian Cancer Cells Through Inhibition of the Phosphatidylinositol 3-Kinase (PI3K)/Akt Pathway

Feng, Xing; Sun, Cong; Luo, Ning; He, Yuanying; Chen, Mengmeng; Ding, Siyu; Liu, Chenghua; Feng, Lijin; Cheng, Zhongping

doi:10.12659/msm.913829

Cited by 21 publications

(12 citation statements)

References 26 publications

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“…Inhibitors of this signaling pathway are candidate drugs for management of this malignancy ( 19 ). Inhibition of PI3K/AKT also enhances the sensitivity of ovarian cancer to cisplatin treatment ( 20 ). In addition, a previous study reported that IMPA2 is involved in the phosphatidylinositol signaling pathway ( 21 ), thus, whether IMPA2 was also involved in the phosphatidylinositol signaling pathway in EOC cancer was investigated.…”

Section: Discussionmentioning

confidence: 99%

Inositol monophosphatase 2 promotes epithelial ovarian cancer cell proliferation and migration by regulating the AKT/mTOR signaling pathway

et al. 2022

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Ovarian cancer is the third most common malignancy in the gynecological reproductive system. Epithelial ovarian cancer (EOC) represents one of the most common subtypes of ovarian cancer. Once diagnosed, the treatment strategies for EOC are limited, and the prognosis is often poor. Recently, inositol monophosphatase 2 (IMPA2) was found to act as an oncogene in cancer development. However, the role of IMPA2 in EOC is unclear. In the present study, the role of IMPA2 in EOC development was assessed through numerous experiments, including knockdown and MTT assays; multiparametric high-content screening; colony formation, apoptosis and Transwell assays, and a xenografted mouse model. IMPA2 was shown to be critical for EOC cell proliferation, growth, migration and tumorigenesis. In addition, experiments showed that knockdown of IMPA2 expression significantly suppressed proliferation and colony formation in the ES-2 and SKOV3 cell lines in vitro. IMPA2 knockdown also suppressed the migration and invasion of the EOC cell lines, and apoptosis was induced. In vivo, IMPA2 knockdown reduced the tumorigenesis of the EOC cells. Mechanistically, IMPA2 knockdown suppressed the AKT/mTOR signaling pathway and epithelial-mesenchymal transition (EMT). Collectively, the results from the present study demonstrated that IMPA2 may be a novel oncogene in EOC cells via regulation of the AKT/mTOR pathway and EMT.

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Section: Discussionmentioning

confidence: 99%

Inositol monophosphatase 2 promotes epithelial ovarian cancer cell proliferation and migration by regulating the AKT/mTOR signaling pathway

et al. 2022

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“…In this study, CAL-27 (CL-0265, Procell, Wuhan, China) and human oral epithelial cells (CP-H203, Procell) were selected for in vitro experiments. In a 37°C cell incubator (51032124, Thermo Fisher Scientific, USA) with 5% CO 2 , CAL-27 was cultured in CAL-27 cell-specific medium (CM-0265, Procell) and human oral epithelial cells in human oral epithelial cell complete medium (CM-h203, Procell), both for 24 h. The cultured CAL-27 cells were assigned to control group and chemotherapy group, among which, cisplatin (10 μ g/mL, 100 μ L) [ 13 ] and paclitaxel (8 μ g/mL, 100 μ L) [ 14 ] were added to the culture medium of chemotherapy group. Eventually, the two groups of cells were cultured in cell incubator for another 24 h.…”

Section: Methodsmentioning

confidence: 99%

miR-214 Modulates the Growth and Migration of Oral Cancer before and after Chemotherapy through Mediating ULK1

Yang

Sun

et al. 2022

Journal of Immunology Research

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The role of miRNAs as crucial components in carcinogenesis has been well documented. However, whether and how miR-214 influences oral cancer cells’ drug resistance remains to be elucidated, and its downstream targets are still under investigation. Hence, this research is aimed at determining miR-214 and ULK1 expression in oral cancer before and after chemotherapy and their correlations with cancer cell growth. Human oral normal epithelial cells and human tongue squamous cell carcinoma CAL-27 cells were cultured to detect miR-214 and ULK1 levels. It was found that before chemotherapy, miR-214 was higher, while ULK1 was underexpressed in CAL-27 cells, versus normal epithelial cells. After chemotherapy, miR-214 decreased obviously in CAL-27 cells, while ULK1 level increased significantly. In addition, autophagy-related genes (Beclin 1, mTOR, and P53) in CAL-27 cells were found to be significantly inhibited before chemotherapy and were obviously increased after chemotherapy. Moreover, to further determine the impacts of miR-214 and ULK1 on oral cancer cell growth after chemotherapy, the two were overexpressed or silenced in CAL-27 cells after transfection. We found that ULK1 could effectively decrease the activity and invasion of CAL-27 cells and increase their apoptosis level, while miR-214 could antagonize its antitumor effect. Therefore, miR-214 can be used as an early prognostic biomarker for oral cancer, and ULK1 is a new candidate therapeutic target.

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“…Furthermore, it was reported that WOG exerted its antitumor potential through ameliorating p53 expression while suppressing tumor growth and glucose transporter 1 (GLUT1) in both in vitro and in vivo ovarian cancer models (Yikai et al, 2018). Besides, this compound was also found to enhance cisplatin sensitivity via suppressing PI3K/Akt pathway (Xing et al, 2019a). Combinatorial treatment of WOG and oridonin showed synergistic cytotoxicity through upregulating p53 expression and downregulating Akt expression in ovarian cancer cells (Chen et al, 2011b).…”

Section: Effect Of Wog In Different Cancersmentioning

confidence: 99%

Wogonin and its analogs for the prevention and treatment of cancer: A systematic review

Banik

Khatoon

Harsha

et al. 2022

Phytotherapy Research

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The medicinal plant Scutellaria baicalensis, commonly known as Chinese skullcap or Huang-Qin, has been used as a traditional medicine for several thousand years. The roots of this plant contain bioactive compounds, such as wogonin (WOG), wogonoside, baicalein, and baicalin. The aim of this article is to evaluate the therapeutic potential and mechanisms of action of WOG against different cancers. Numerous in vitro and in vivo studies have revealed that WOG exerts immense therapeutic potential against bladder cancer, breast cancer, cholangiocarcinoma, cervical cancer, colorectal cancer, gallbladder cancer, gastric cancer, glioblastoma, head and neck cancer, hepatic cancer, leukemia, lung cancer, lymphoma, melanoma, multiple myeloma, neuroblastoma, osteosarcoma, ovarian cancer, pancreatic cancer, prostate cancer, and renal cancer by regulating various cell signaling pathways. WOG, in combination with established chemotherapeutic drugs, improves the efficacy of treatment and lowers toxicity. Nevertheless, human trials are warranted to validate these findings.Numerous preclinical studies, combined with an extensive margin of safety and no severe side effects, underscore WOG's therapeutic potential as an anticancer drug.

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Wogonin Increases Cisplatin Sensitivity in Ovarian Cancer Cells Through Inhibition of the Phosphatidylinositol 3-Kinase (PI3K)/Akt Pathway

Cited by 21 publications

References 26 publications

Inositol monophosphatase 2 promotes epithelial ovarian cancer cell proliferation and migration by regulating the AKT/mTOR signaling pathway

Inositol monophosphatase 2 promotes epithelial ovarian cancer cell proliferation and migration by regulating the AKT/mTOR signaling pathway

miR-214 Modulates the Growth and Migration of Oral Cancer before and after Chemotherapy through Mediating ULK1

Wogonin and its analogs for the prevention and treatment of cancer: A systematic review

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