Mei‐Yin Zhang

Sun Yat-sen University

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Hui‐Yun Wang

Sun Yat-sen University

Huizhong Zhang

Beijing University of Chinese Medicine

Shi‐Juan Mai

Sun Yat-sen University

Guoliang Huang

Guangdong Medical College

Wei‐Hua Jia

Sun Yat-sen University

Ming Shi

Sun Yat-sen University

Yunfei Yuan

Sun Yat-sen University

Rongrong Wei

Capital Medical University

Binkui Li

Sun Yat-sen University Cancer Center

Qingming Zhou

Hunan Agricultural University

Cooperative Institutions

Sun Yat-sen University

Sun Yat-sen University Cancer Center

State Key Laboratory of Oncology in South China

Harbin Medical University

Third Affiliated Hospital of Harbin Medical University

Southern Medical University

Chinese Academy of Medical Sciences & Peking Union Medical College

Chinese Academy of Sciences

Guangzhou Medical University

Peking University

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Supplementary Figure 2 from Clinical Significance and Prognostic Value of microRNA Expression Signatures in Hepatocellular Carcinoma

Rongrong Wei Guoliang Huang Mei‐Yin Zhang Binkui Li Huizhong Zhang

PDF file, 131K, The relationship between 20-miRNA signature risk score and survival status of HCC patients in combination of training and test sets.

Value (mathematics)

Signature (topology)

10.1158/1078-0432.22445813

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Supplementary Table 3 from Clinical Significance and Prognostic Value of microRNA Expression Signatures in Hepatocellular Carcinoma

Rongrong Wei Guoliang Huang Mei‐Yin Zhang Binkui Li Huizhong Zhang

PDF file, 132K, Differential expression of miRNAs between clinical features.

Value (mathematics)

Expression (computer science)

Table (database)

Clinical Significance

10.1158/1078-0432.22445798

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Supplementary Table 1 from Clinical Significance and Prognostic Value of microRNA Expression Signatures in Hepatocellular Carcinoma

Rongrong Wei Guoliang Huang Mei‐Yin Zhang Binkui Li Huizhong Zhang

PDF file, 97K, Overall survival (OS) and disease-free survival (DFS) in Training set, Test Set and Independent Cohort.

Value (mathematics)

Clinical Significance

Table (database)

Expression (computer science)

10.1158/1078-0432.22445804

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miR-601 is a prognostic marker and suppresses cell growth and invasion by targeting PTP4A1 in breast cancer

Biomedicine & Pharmacotherapy (2016)

Jing-Ye Hu Wei Yi Xuan Wei Mei‐Yin Zhang Rui‐Hua Xu

Ectopic expression

CA 15-3

10.1016/j.biopha.2016.02.014

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Citations (40)

Two somatic mutations in the androgen receptor N-terminal domain are oncogenic drivers in hepatocellular carcinoma

Communications Biology (2024)

Qiannan Ren Danhui Huang Xiaonan Zhang Yue-Ning Wang Yufeng Zhou

Abstract The androgen receptor ( AR ) plays an important role in male-dominant hepatocellular carcinoma, and specific acquired somatic mutations of AR have been observed in HCC patients. Our previous research have established the role of AR wild type as one of the key oncogenes in hepatocarcinogenesis. However, the role of hepatic acquired somatic mutations of AR remains unknown. In this study, we identify two crucial acquired somatic mutations, Q62L and E81Q , situated close to the N-terminal activation function domain-1 of AR . These mutations lead to constitutive activation of AR , both independently and synergistically with androgens, making them potent driver oncogene mutations. Mechanistically, these N-terminal AR somatic mutations enhance de novo lipogenesis by activating sterol regulatory element-binding protein-1 and promote glycogen accumulation through glycogen phosphorylase, brain form, thereby disrupting the AMPK pathway and contributing to tumorigenesis. Moreover, the AR mutations show sensitivity to the AMPK activator A769662. Overall, this study establishes the role of these N- terminal hepatic mutations of AR as highly malignant oncogenic drivers in hepatocarcinogenesis and highlights their potential as therapeutic targets for patients harboring these somatic mutations.

10.1038/s42003-023-05704-2

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High expression of miR-221 indicates poor prognosis in patients with intrahepatic cholangiocarcinoma

Chin J Hepat Surg(Electronic Edition) (2019)

Yuhao Tang Juncheng Wang Mei‐Yin Zhang Ying‐Qin Zhu Jinbin Chen

Objective To observe the expression profile of miRNAs in intrahepatic cholangiocarcinoma (ICC), and to explore its value in predicting the survival and prognosis of ICC patients. Methods The tissue specimens were obtained from 134 patients with ICC or with combined hepatocellular and cholangiocarcinoma (cHCC-CC) receiving surgical resection in Sun Yat-sen University Cancer Center from April 2000 to September 2014. Normal bile duct tissues were collected from 5 patients as controls. The expression levels of miR-221, miR-675, miR-1248 and miR-1292 in tumor tissues were quantitatively detected by qRT-PCR and the clinicopathological characteristics were analyzed. The informed consents of all patients were obtained and the local ethical committee approval was received. Correlation analysis was performed by Chi-square test. Survival analysis was performed by using Kaplan-Meier method and Log-rank test. Factors that may affect the prognosis were subject to univariate and multivariate analyses using Cox's proportional hazard model. Results Among 134 patients, ICC patients accounted for 63.4% (85/134) and cHCC-CC patients 36.6% (49/134). The proportion of patients with high expression of miR-221, miR-675, miR-1248 and miR-1292 in tumor tissues were 43.3%, 44.0%, 77.6% and 59.7%, respectively. The expression level of miR-221 was significantly correlated with the metastasis of tumor lymph node, and patients with high expression presented with a high incidence of lymph node metastasis (χ2=7.65, P<0.05). Multivariate analysis demonstrated that high expression of miR-221 was an independent risk factor for the overall survival of patients (HR=1.878, 95%CI: 1.135-3.106; P<0.05). The median overall survival time of patients with high expression of miR-221 was 14.5 months and 34.0 months for those with low expression of miR-221. The prognosis was worse for patients with high expression (χ2=8.87, P<0.05). Conclusions High expression of miR-221 is an independent risk factor for clinical prognosis of ICC patients, indicating a poor prognosis in ICC patients. Key words: Bile duct neoplasms; Intrahepatic cholangiocarcinoma; MicroRNAs; Prognosis

Intrahepatic Cholangiocarcinoma

Univariate analysis

10.3877/cma.j.issn.2095-3232.2019.06.015

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Supplementary Table 4 from Clinical Significance and Prognostic Value of microRNA Expression Signatures in Hepatocellular Carcinoma

Rongrong Wei Guoliang Huang Mei‐Yin Zhang Binkui Li Huizhong Zhang

PDF file, 125K, Univariate and multivariate analysis of features associated with overall survival.

Univariate

Table (database)

Value (mathematics)

Univariate analysis

Clinical Significance

Expression (computer science)

10.1158/1078-0432.22445795

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Cholesterol inhibition enhances antitumor response of gilteritinib in lung cancer cells

Research Square (Research Square) (2024)

Shi‐Juan Mai Chao‐Yue Sun Di Cao Yue-Ning Wang Qiannan Ren

Abstract Repositioning approved antitumor drugs for different cancers is a cost-effective approach. Gilteritinib was FDA-approved for the treatment of FLT3-mutated acute myeloid leukaemia in 2018. However, the theraputic effects and mechanism of Gilteritinib on other malignancies remains to be defined. In this study, we identified that gilteritinib has an inhibitory effect on lung cancer cells (LCCs) without FLT3 mutation in vitro and in vivo. Unexpectedly, we found that gilteritinib induces cholesterol accumulation in LCCs via upregulating cholesterol biosynthetic genes and inhibiting cholesterol efflux. This gilteritinib-induced cholesterol accumulation not only attenuates the antitumor effect of gilteritinib but also induces gilteritinib-resistance in LCCs. However, when cholesterol synthesis was prevented by squalene epoxidase (SQLE) inhibitor NB-598, both LCCs and gilteritinib-resistant LCCs became sensitive to gilteritinib. More important, the natural cholesterol inhibitor 25-hydroxycholesterol (25HC) can suppress cholesterol biosynthesis and increase cholesterol efflux in LCCs. Consequently, 25HC treatment significantly increases the cytotoxicity of gilteritinib on LCCs, which can be rescued by addition of exogenous cholesterol. In a xenograft model, the combination of gilteritinib and 25HC showed significantly better efficacy than either monotherapy in suppressing lung cancer growth, without obvious general toxicity. Thus, our findings identify an increase in cholesterol induced by gilteritinib as a mechanism for LCC survival, and highlight the potential of combining gilteritinib with cholesterol-lowering drugs to treat lung cancer.

Efflux

10.21203/rs.3.rs-4135023/v1

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Rapamycin and trametinib: a rational combination for treatment of NSCLC

International Journal of Biological Sciences (2021)

Chao‐Yue Sun Yizhuo Li Di Cao Yufeng Zhou Mei‐Yin Zhang

Mammalian target of rapamycin (mTOR) is one of the most commonly activated pathways in human cancers, including lung cancer.Targeting mTOR with molecule inhibitors is considered as a useful therapeutic strategy.However, the results obtained from the clinical trials with the inhibitors so far have not met the original expectations, largely because of the drug resistance.Thus, combined or multiple drug therapy can bring about more favorable clinical outcomes.Here, we found that activation of ERK pathway was responsible for rapamycin drug resistance in non-small-cell lung cancer (NSCLC) cells.Accordingly, rapamycin-resistant NSCLC cells were more sensitive to ERK inhibitor (ERKi), trametinib, and in turn, trametinib-resistant NSCLC cells were also susceptible to rapamycin.Combining rapamycin with trametinib led to a potent synergistic antitumor efficacy, which induced G1-phase cycle arrest and apoptosis.In addition, rapamycin synergized with another ERKi, MEK162, and in turn, trametinib synergized with other mTORi, Torin1 and OSI-027.Mechanistically, rapamycin in combination with trametinib resulted in a greater decrease of phosphorylation of AKT, ERK, mTOR and 4EBP1.In xenograft mouse model, co-administration of rapamycin and trametinib caused a substantial suppression in tumor growth without obvious drug toxicity.Overall, our study identifies a reasonable combined strategy for treatment of NSCLC.

Trametinib

Sirolimus

Everolimus

10.7150/ijbs.62752

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Supplementary Figure Legends from Clinical Significance and Prognostic Value of microRNA Expression Signatures in Hepatocellular Carcinoma

Rongrong Wei Guoliang Huang Mei‐Yin Zhang Binkui Li Huizhong Zhang

PDF file, 40K.

Value (mathematics)

Clinical Significance

Expression (computer science)

10.1158/1078-0432.22445807.v1

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