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2. Neoadjuvant everolimus in renal angiomyolipoma with or without tuberous sclerosis complex: Results from a multicenter, retrospective study.

Author

Su, Ruopeng, Huang, Tingxuan, Gu, Liangyou, Bao, Yige, Liu, Zhihong, Dao, Pinghong, Yao, Lin, Hu, Xiaoyi, Fu, Guanghou, Wu, Jitao, Tricard, Thibault, Wu, Guangyu, Chen, Minfeng, Li, Chancan, Huang, Zhiyang, Zheng, Bing, Chen, Yonghui, Xue, Wei, Guo, Gang, and Dong, Pei

Subjects
TUBEROUS sclerosis, NEOADJUVANT chemotherapy, KIDNEY physiology, ANGIOMYOLIPOMA, EVEROLIMUS, NEPHRECTOMY
Abstract

Objectives: To assess the efficacy and safety of preoperative neoadjuvant everolimus in renal angiomyolipomas (AML) patients with or without Tuberous Sclerosis Complex (TSC). Materials and Methods: This multi‐institutional retrospective study enrolled renal AML patients who underwent partial nephrectomy (PN) or total nephrectomy after receiving at least 1 month of pre‐operative everolimus. Imaging evaluations were collected before and after treatment, along with demographic, surgical, and follow‐up information. The primary outcome was tumor volume reduction of ≥25%, with additional outcomes including recurrence, perioperative outcomes, renal function, and safety. Results: From January 2015 to July 2022, 68 renal AML patients were studied—41 with TSC and 27 without. During everolimus treatment, 61.0% (25/41) of TSC patients and 44.4% (12/27) of non‐TSC patients achieved tumor reduction of ≥25%. Additionally, 41.5% (17/41) of TSC patients and 18.5% (5/27) of non‐TSC patients achieved a ≥ 50% reduction. Three TSC patients and 1 non‐TSC patient discontinued treatment due to side‐effects. Most patients (92.7% TSC, 85.2% non‐TSC) underwent PN. After everolimus treatment, the necessary total nephrectomy decreased to 41.2% (7/17) from baseline. Postoperatively, 1 grade 3 and 3 grade 2 complications occurred, with no grade 4 or 5 complications. After a median follow‐up of 24 months, only 1 TSC patient recurred with a diameter >3 cm. Retrospective nature is the major limitation of this study. Conclusion: Everolimus was effective and well‐tolerated in neoadjuvant treatment for renal AML, especially in TSC patients. This neoadjuvant combination strategy of everolimus and PN could effectively controls recurrence and preserves renal function. [ABSTRACT FROM AUTHOR]

Published
2024
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3. Survival after radical cystectomy for bladder cancer: Multicenter comparison between minimally invasive and open approaches

Author

Xie, Weibin, Bi, Junming, Wei, Qiang, Han, Ping, Song, Dongkui, Shi, Lei, Ye, Dingwei, Shen, Yijun, Gou, Xin, He, Weiyang, Wang, Shaogang, Liu, Zheng, Fan, Jinhai, Wu, Kaijie, Chen, Zhiwen, Zhou, Xiaozhou, Kong, Chuize, Liu, Yang, Liu, Chunxiao, Xu, Abai, Jin, Baiye, Fu, Guanghou, Xue, Wei, Chen, Haige, Pan, Tiejun, Tu, Zhong, Lin, Tianxin, and Huang, Jian

Published
2020
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4. Data from SETD2 Deficiency Confers Sensitivity to Dual Inhibition of DNA Methylation and PARP in Kidney Cancer

Author

Zhou, Xinyi, primary, Sekino, Yohei, primary, Li, Hong-Tao, primary, Fu, Guanghou, primary, Yang, Zhi, primary, Zhao, Shuqing, primary, Gujar, Hemant, primary, Zu, Xiongbing, primary, Weisenberger, Daniel J., primary, Gill, Inderbir S., primary, Tulpule, Varsha, primary, D’souza, Anishka, primary, Quinn, David I., primary, Han, Bo, primary, and Liang, Gangning, primary

Published
2023
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5. Supplemental Figure S4 from SETD2 Deficiency Confers Sensitivity to Dual Inhibition of DNA Methylation and PARP in Kidney Cancer

Author

Zhou, Xinyi, primary, Sekino, Yohei, primary, Li, Hong-Tao, primary, Fu, Guanghou, primary, Yang, Zhi, primary, Zhao, Shuqing, primary, Gujar, Hemant, primary, Zu, Xiongbing, primary, Weisenberger, Daniel J., primary, Gill, Inderbir S., primary, Tulpule, Varsha, primary, D’souza, Anishka, primary, Quinn, David I., primary, Han, Bo, primary, and Liang, Gangning, primary

Published
2023
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6. Supplementary Figure legends from SETD2 Deficiency Confers Sensitivity to Dual Inhibition of DNA Methylation and PARP in Kidney Cancer

Author

Zhou, Xinyi, primary, Sekino, Yohei, primary, Li, Hong-Tao, primary, Fu, Guanghou, primary, Yang, Zhi, primary, Zhao, Shuqing, primary, Gujar, Hemant, primary, Zu, Xiongbing, primary, Weisenberger, Daniel J., primary, Gill, Inderbir S., primary, Tulpule, Varsha, primary, D’souza, Anishka, primary, Quinn, David I., primary, Han, Bo, primary, and Liang, Gangning, primary

Published
2023
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7. Supplementary Table 1 from SETD2 Deficiency Confers Sensitivity to Dual Inhibition of DNA Methylation and PARP in Kidney Cancer

Author

Zhou, Xinyi, primary, Sekino, Yohei, primary, Li, Hong-Tao, primary, Fu, Guanghou, primary, Yang, Zhi, primary, Zhao, Shuqing, primary, Gujar, Hemant, primary, Zu, Xiongbing, primary, Weisenberger, Daniel J., primary, Gill, Inderbir S., primary, Tulpule, Varsha, primary, D’souza, Anishka, primary, Quinn, David I., primary, Han, Bo, primary, and Liang, Gangning, primary

Published
2023
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8. Supplementary Table 2 from SETD2 Deficiency Confers Sensitivity to Dual Inhibition of DNA Methylation and PARP in Kidney Cancer

Author

Zhou, Xinyi, primary, Sekino, Yohei, primary, Li, Hong-Tao, primary, Fu, Guanghou, primary, Yang, Zhi, primary, Zhao, Shuqing, primary, Gujar, Hemant, primary, Zu, Xiongbing, primary, Weisenberger, Daniel J., primary, Gill, Inderbir S., primary, Tulpule, Varsha, primary, D’souza, Anishka, primary, Quinn, David I., primary, Han, Bo, primary, and Liang, Gangning, primary

Published
2023
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10. SETD2 Deficiency Confers Sensitivity to Dual Inhibition of DNA Methylation and PARP in Kidney Cancer

Author

Zhou, Xinyi, primary, Sekino, Yohei, additional, Li, Hong-Tao, additional, Fu, Guanghou, additional, Yang, Zhi, additional, Zhao, Shuqing, additional, Gujar, Hemant, additional, Zu, Xiongbing, additional, Weisenberger, Daniel J., additional, Gill, Inderbir S., additional, Tulpule, Varsha, additional, D’souza, Anishka, additional, Quinn, David I., additional, Han, Bo, additional, and Liang, Gangning, additional

Published
2023
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18. Albumin levels predict prognosis in advanced renal cell carcinoma treated with tyrosine kinase inhibitors: a systematic review and meta-analysis

Author

Zhou, Xinyi, primary, Fu, Guanghou, additional, Zu, Xiongbing, additional, Xu, Zhijie, additional, Li, Hong-Tao, additional, D'souza, Anishka, additional, Tulpule, Varsha, additional, Quinn, David I, additional, Bhowmick, Neil A, additional, Weisenberger, Daniel J, additional, Liang, Gangning, additional, and Chen, Jinbo, additional

Published
2022
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19. Microfluidic Assaying of Circulating Tumor Cells and Its Application in Risk Stratification of Urothelial Bladder Cancer

Author

Congcong Xu, Zhijie Xu, Kuang Hong Neoh, Ray P. S. Han, Fu Guanghou, Yun Dai, Kok Suen Cheng, Junjie Tian, Yukun Sun, Anqi Chen, Xiaoyi Chen, and Baiye Jin

Subjects
0301 basic medicine, Oncology, medicine.medical_specialty, Cancer Research, microfluidics, Disease, risk stratification, circulating tumor cells, 03 medical and health sciences, 0302 clinical medicine, Circulating tumor cell, Internal medicine, Biopsy, medicine, Pathological, RC254-282, Original Research, Bladder cancer, medicine.diagnostic_test, business.industry, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, Gold standard (test), medicine.disease, 030104 developmental biology, 030220 oncology & carcinogenesis, Risk stratification, Biomarker (medicine), bladder cancer, biomarker, business
Abstract

Bladder cancer is characterized by its frequent recurrence and progression. Effective treatment strategies need to be based on an accurate risk stratification, in which muscle invasiveness and tumor grade represent the two most important factors. Traditional imaging techniques provide preliminary information about muscle invasiveness but are lacking in terms of accuracy. Although as the gold standard, pathological biopsy is only available after the surgery and cannot be performed longitudinally for long-term surveillance. In this work, we developed a microfluidic approach that interrogates circulating tumor cells (CTCs) in the peripheral blood of bladder cancer patients to reflect the risk stratification of the disease. In a cohort of 48 bladder cancer patients comprising 33 non-muscle invasive bladder cancer (NMIBC) cases and 15 muscle invasive bladder cancer (MIBC) cases, the CTC count was found to be considerably higher in the MIBC group compared with the NMIBC group (4.67 vs. 1.88 CTCs/3 mL, P=0.019), and was significantly higher in high-grade bladder cancer patients verses low-grade bladder cancer patients (3.69 vs. 1.18 CTCs/3mL, P=0.024). This microfluidic assay of CTCs is believed to be a promising complementary tool for the risk stratification of bladder cancer.

Published
2021

21. Microfluidic Assaying of Circulating Tumor Cells and its Correlation with Muscle Invasiveness and Tumor Grade of Urothelial Bladder Cancer

Author

Xiaoyi Chen, Baiye Jin, Junjie Tian, Anqi Chen, Yun Dai, Ray P. S. Han, Fu Guanghou, Zhijie Xu, Yukun Sun, Congcong Xu, Kuang Hong Neoh, and Kok Suen Cheng

Subjects
Tumor grade, Circulating tumor cell, Bladder cancer, business.industry, Cancer research, Medicine, business, medicine.disease
Abstract

Background: Bladder cancer is characterized by its frequent recurrence and progression. Effective treatment strategies need to be based on an accurate risk stratification, in which muscle invasiveness and tumor grade represent the two most important factors. Traditional imaging techniques provide preliminary information about muscle invasiveness but are lacking in terms of accuracy. Although as the gold standard, pathological biopsy is only available after the surgery and cannot be performed longitudinally for long-term surveillance. Methods: In this work, we developed a microfluidic approach that interrogates circulating tumor cells (CTCs) in the peripheral blood of bladder cancer patients to reflect the risk stratification of the disease. Results：In a cohort of 48 bladder cancer patients comprising 33 non-muscle invasive bladder cancer (NMIBC) cases and 15 muscle invasive bladder cancer (MIBC) cases, the CTC count was found to be considerably higher in the MIBC group compared with the NMIBC group (4.67 vs. 1.88 CTCs/3 mL, P=0.019), and was significantly higher in high-grade bladder cancer patients verses low-grade bladder cancer patients (3.69 vs. 1.18 CTCs/3mL, P=0.024). Conclusions: This microfluidic assay of CTCs is believed to be a promising complementary tool for the risk stratification of bladder cancer.Trial registration: This research was conducted under the approval of the Ethics Committee of the First Affiliated Hospital at Zhejiang University School of Medicine with the Registration No. 2015-218.

Published
2021
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22. Cisplatin Inhibits Bladder Cancer Proliferation Through cGAS-STING Pathway

Author

Junjie Su, Xiaoyi Chen, Hao Pan, Jin Baiye, Junjie Tian, Fu Guanghou, Zhijie Xu, Congcong Xu, and Yue Shi

Subjects
Cisplatin, Sting, Bladder cancer, business.industry, Cancer research, Medicine, urologic and male genital diseases, business, medicine.disease, medicine.drug
Abstract

Background Cisplatin is a commonly used adjuvant chemotherapy for advanced bladder cancer, but its immune related mechanism is still unclear. Exploration the immune effects of cisplatin in bladder cancer would complement the comprehensive mechanism of cisplatin and provide the basis for combination therapy of cisplatin and immunotherapy in bladder cancer. Methods We confirmed the immune effects of cisplatin on T24 and TCCSUP bladder cancer cell lines in vitro and exploration the important function of these immune effects in bladder cancer microenvironment in mice tumor model. Results We found cisplatin induced immune response in bladder cancer by RNA sequencing, and validated cGAS-STING signal was deeply involved in this response. Cisplatin induced cGAS-STING signal inhibited the proliferation of bladder cancer and increased the infiltration percentages of CD8 + T cells and dendritic cells in transplantation mice tumor model. Accumulation of dsDNA and the release of chromatin bound cGAS are important to activate downstream STING. Conclusion Our findings indicated a cisplatin related immune effects in bladder cancer, cisplatin combined with immunotherapy might have a synergistic effect for bladder cancer therapy.

Published
2020
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24. Microfluidic Assaying of Circulating Tumor Cells and its Correlation with Muscle Invasiveness and Tumor Grade of Urothelial Bladder Cancer

Author

Fu, Guanghou, primary, Cheng, Kok Suen, additional, Chen, Anqi, additional, Xu, Zhijie, additional, Chen, Xiaoyi, additional, Tian, Junjie, additional, Xu, Congcong, additional, Sun, Yukun, additional, Neoh, Kuang Hong, additional, Dai, Yun, additional, Han, Ray P.S., additional, and Jin, Baiye, additional

Published
2021
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25. A Novel DNA Methylation Signature as an Independent Prognostic Factor in Muscle-Invasive Bladder Cancer

Author

Xu, Zhijie, primary, Gujar, Hemant, additional, Fu, Guanghou, additional, Ahmadi, Hamed, additional, Bhanvadia, Sumeet, additional, Weisenberger, Daniel J., additional, Jin, Baiye, additional, Gill, Parkash S., additional, Gill, Inderbir, additional, Daneshmand, Siamak, additional, Siegmund, Kimberly D., additional, and Liang, Gangning, additional

Published
2021
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30. Detection of Urothelial Bladder Carcinoma via Microfluidic Immunoassay and Single-Cell DNA Copy-Number Alteration Analysis of Captured Urinary-Exfoliated Tumor Cells

Author

Yukun Sun, Anqi Chen, Kok Suen Cheng, Xiaoyi Chen, Tanxiao Huang, Baiye Jin, Shifu Chen, Yun Dai, Kuang Hong Neoh, Ming Liu, Zhewen Tang, Qibo Wang, Zhijie Xu, Ray P. S. Han, Fu Guanghou, and Jing Jin

Subjects
0301 basic medicine, Male, Cancer Research, DNA Copy Number Variations, Urinary system, Microfluidics, Urinary Bladder, Sensitivity and Specificity, 03 medical and health sciences, Antigens, Neoplasm, Cytology, Cell Line, Tumor, medicine, Carcinoma, Humans, Aged, Immunoassay, Bladder cancer, medicine.diagnostic_test, business.industry, Cancer, Cystoscopy, DNA, Middle Aged, medicine.disease, 030104 developmental biology, Oncology, Urinary Bladder Neoplasms, Tumor progression, Case-Control Studies, Cancer research, Female, Neoplasm Recurrence, Local, Single-Cell Analysis, business
Abstract

The increasing incidence of bladder cancer and its high rate of recurrence over a 5-year period necessitate the need for diagnosis and surveillance amelioration. Cystoscopy and urinary cytology are the current tools, and molecular techniques such as BTA stat, NMP22, survivin mRNA, and urovysion FISH have attracted attention; however, they suffer from insufficient sensitivity or specificity. We developed a novel microfluidic approach for harvesting intact urinary-exfoliated tumor cells (UETC), either individually or in clusters, in a clean and segregated environment, which is crucial to minimize cross-contamination and misreads. To reliably and accurately identify UETC, our quantitative immunoassay involved concurrent use of two oncoproteins CK20 and CD44v6 antigen. CK20 is an intermediate filament protein overexpressed in urothelial tumors, and CD44v6 is a membrane adhesion molecule closely associated with cell invasion, tumor progression, and metastatic spread. Single-cell whole-genome sequencing on 12 captured UETCs and copy number alteration analysis showed that 11/12 (91.7%) of the immunofluorescence-identified UETCs possessed genomic instability. A total of 79 patients with bladder cancer and 43 age-matched normal controls (NC) were enrolled in the study. We detected considerably higher UETC counts in patients with bladder cancer versus the NC group [53.3 (10.7–1001.9) vs. 0.0 (0–3.0) UETCs/10 mL; P < 0.0001]. For bladder cancer detection, a stratified 10-fold cross-validation of training data reveals an overall predictive accuracy of 0.84 [95% confidence interval (CI), 0.76–0.93] with an 89.8% (95% CI, 71.5%–86.4%) for sensitivity and 71.5% (95% CI, 59.7%–83.3%) for specificity. Overall, the microfluidic immunoassay demonstrates increased sensitivity and specificity compared with other techniques for the detection of bladder cancer. Significance: A unique and promising diagnostic assay for bladder cancer is proposed with potential clinical utility as a complement for cytology. Cancer Res; 78(14); 4073–85. ©2018 AACR.

Published
2017

32. Detection of Urothelial Bladder Carcinoma via Microfluidic Immunoassay and Single-Cell DNA Copy-Number Alteration Analysis of Captured Urinary-Exfoliated Tumor Cells

Author

Chen, Anqi, primary, Fu, Guanghou, additional, Xu, Zhijie, additional, Sun, Yukun, additional, Chen, Xiaoyi, additional, Cheng, Kok Suen, additional, Neoh, Kuang Hong, additional, Tang, Zhewen, additional, Chen, Shifu, additional, Liu, Ming, additional, Huang, Tanxiao, additional, Dai, Yun, additional, Wang, Qibo, additional, Jin, Jing, additional, Jin, Baiye, additional, and Han, Ray P.S., additional

Published
2018
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33. Current status of diagnosis and treatment of bladder cancer in China – Analyses of Chinese Bladder Cancer Consortium database

Author

Li, Kaiwen, Lin, Tianxin, Xue, Wei, Mu, Xin, Xu, Enci, Yang, Xu, Chen, Fubao, Li, Guangyong, Ma, Lulin, Wang, Guoliang, Liang, Chaozhao, Shi, Haoqiang, Li, Ming, Tang, Mao, Xue, Xueyi, Lv, Yisong, Deng, Yaoliang, Li, Chengyang, Chen, Zhiwen, Zhou, Xiaozhou, Jin, Fengshuo, Liu, Xudong, Wei, Jinxin, Shi, Lei, Gou, Xin, He, Weiyang, Zhou, Liqun, Cai, Lin, Jin, Baiye, Fu, Guanghou, Kong, Xiangbo, Sun, Hongyan, Tian, Ye, Feng, Lang, Pan, Tiejun, Wu, Yiyi, Wang, Dongwen, Hao, Hailong, Shi, Benkang, Zhu, Yaofeng, Wei, Qiang, Han, Ping, Wu, Changli, Tian, Dawei, Ye, Zhangqun, Liu, Zheng, Wang, Zhiping, Tian, Junqiang, Qi, Lin, Chen, Minfeng, Li, Wei, Qi, Jinchun, Wang, Gongxian, Fu, Longlong, Sun, Zhaolin, Luo, Guangheng, Shen, Zhoujun, Zhu, Zhaowei, Xing, Jinchun, Wu, Zhun, Wei, Dong, Chen, Xin, Na, Yanqun, Guo, Hongfeng, Wang, Chunxi, Lu, Zhihua, Kong, Chuize, Liu, Yang, Yang, Jin, Hu, Jianyun, Gao, Xin, Li, Jielin, Yin, Changjun, Li, Pu, Chen, Shan, Du, Zhen, Li, Jiongming, Yan, Yongji, Zhang, Xu, Huang, Shuang, Zhou, Fangjian, Zhang, Zhiling, Sun, Yinghao, Zeng, Shuxiong, Cen, Song, Zhou, Jiaquan, Li, Hanzhong, Wen, Jin, and Huang, Jian

Published
2015
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36. WITHDRAWN: Current status of diagnosis and treatment of bladder cancer in China – Analyses of Chinese Bladder Cancer Consortium Database

Author

Li, Kaiwen, primary, Lin, Tianxin, additional, Xue, Wei, additional, Mu, Xin, additional, Xu, Enci, additional, Yang, Xu, additional, Chen, Fubao, additional, Li, Guangyong, additional, Ma, Lulin, additional, Wang, Guoliang, additional, Liang, Chaozhao, additional, Shi, Haoqiang, additional, Li, Ming, additional, Tang, Mao, additional, Xue, Xueyi, additional, Lv, Yisong, additional, Deng, Yaoliang, additional, Li, Chengyang, additional, Chen, Zhiwen, additional, Zhou, Xiaozhou, additional, Jin, Fengshuo, additional, Liu, Xudong, additional, Wei, Jinxin, additional, Shi, Lei, additional, Gou, Xin, additional, He, Weiyang, additional, Zhou, Liqun, additional, Cai, Lin, additional, Xie, Liping, additional, Fu, Guanghou, additional, Kong, Xiangbo, additional, Sun, Hongyan, additional, Tian, Ye, additional, Feng, Lang, additional, Pan, Tiejun, additional, Wu, Yiyi, additional, Wang, Dongwen, additional, Hao, Hailong, additional, Shi, Benkang, additional, Zhu, Yaofeng, additional, Wei, Qiang, additional, Han, Ping, additional, Wu, Changli, additional, Tian, Dawei, additional, Ye, Zhangqun, additional, Liu, Zheng, additional, Wang, Zhiping, additional, Tian, Junqiang, additional, Qi, Lin, additional, Chen, Minfeng, additional, Li, Wei, additional, Qi, Jinchun, additional, Wang, Gongxian, additional, Fu, Longlong, additional, Sun, Zhaolin, additional, Luo, Guangheng, additional, Shen, Zhoujun, additional, Zhu, Zhaowei, additional, Xing, Jinchun, additional, Wu, Zhun, additional, Wei, Dong, additional, Chen, Xin, additional, Na, Yanqun, additional, Guo, Hongfeng, additional, Wang, Chunxi, additional, Lu, Zhihua, additional, Kong, Chuize, additional, Liu, Yang, additional, Yang, Jin, additional, Hu, Jianyun, additional, Gao, Xin, additional, Li, Jielin, additional, Yin, Changjun, additional, Li, Pu, additional, Chen, Shan, additional, Du, Zhen, additional, Li, Jiongming, additional, Yan, Yongji, additional, Zhang, Xu, additional, Huang, Shuang, additional, Zhou, Fangjian, additional, Zhang, Zhiling, additional, Sun, Yinghao, additional, Zeng, Shuxiong, additional, Cen, Song, additional, Zhou, Jiaquan, additional, Li, Hanzhong, additional, Wen, Jin, additional, and Huang, Jian, additional

Published
2015
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38. Mitofusin-2 is a novel direct target of p53

Author

Wang, Weilin, primary, Cheng, Xiaofei, additional, Lu, Jianju, additional, Wei, Jianfeng, additional, Fu, Guanghou, additional, Zhu, Feng, additional, Jia, Changku, additional, Zhou, Lin, additional, Xie, Haiyang, additional, and Zheng, Shusen, additional

Published
2010
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40. NOP2-mediated 5-methylcytosine modification of APOL1 messenger RNA activates PI3K-Akt and facilitates clear cell renal cell carcinoma progression.

Author

Tian J, Gao J, Cheng C, Xu Z, Chen X, Wu Y, Fu G, and Jin B

Subjects
Humans, Cell Line, Tumor, Mice, 5-Methylcytosine metabolism, Animals, Cell Proliferation genetics, Mice, Nude, Male, Disease Progression, Female, Gene Expression Regulation, Neoplastic, Signal Transduction, Cell Movement genetics, Carcinoma, Renal Cell metabolism, Carcinoma, Renal Cell genetics, Carcinoma, Renal Cell pathology, Proto-Oncogene Proteins c-akt metabolism, Phosphatidylinositol 3-Kinases metabolism, Kidney Neoplasms metabolism, Kidney Neoplasms genetics, Kidney Neoplasms pathology, Apolipoprotein L1 metabolism, Apolipoprotein L1 genetics, RNA, Messenger metabolism, RNA, Messenger genetics
Abstract

Background: By regulating the functions of multiple RNAs, 5-methylcytosine (m 5 C) RNA methylation, particularly mediated by NOP2, is involved in tumorigenesis and developments. However, the specific functions and potential mechanisms of m 5 C, especially involving NOP2, in clear-cell renal cell carcinoma (ccRCC), remain unclear. Methods: NOP2 expression in cell lines and patient tissues was detected using western blotting, quantitative real-time polymerase chain reaction (RT-qPCR), and immunohistochemistry. The biological effects of NOP2 on ccRCC cells were investigated through a series of in vitro and in vivo experiments. To explore the potential regulatory mechanisms by which NOP2 affects ccRCC progression, m 5 C bisulfite sequencing, RNA-sequencing, RNA immunoprecipitation and methylated RNA immunoprecipitation (RIP/MeRIP) RT-qPCR assay, luciferase reporter assay, RNA stability assay, and bioinformatic analysis were performed. Results: NOP2 expression was significantly upregulated in ccRCC tissues and was associated with poor prognosis. Moreover, loss-of-function and gain-of-function assays demonstrated that NOP2 altered ccRCC cell proliferation, migration, and invasion. Mechanistically, NOP2 stimulated m 5 C modification of apolipoprotein L1 (APOL1) mRNA, and m 5 C reader YBX1 stabilized APOL1 mRNA through recognizing and binding to m 5 C site in the 3'-untranslated regions. Silencing APOL1 expression inhibited ccRCC cell proliferation in vitro and tumor formation in vivo . Furthermore, NOP2/APOL1 affected ccRCC progression via the PI3K-Akt signaling pathway. Conclusion: NOP2 functions as an oncogene in ccRCC by promoting tumor progression through the m 5 C-dependent stabilization of APOL1, which in turn regulates the PI3K-Akt signaling pathway, suggesting a potential therapeutic target for ccRCC., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

Published
2024
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