Xingkang Jiang

Second Hospital of Tianjin Medical University

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Shanqi Guo

First Teaching Hospital of Tianjin University of Traditional Chinese Medicine

Yong Xu

Tianjin Medical University

Ranlu Liu

Second Hospital of Tianjin Medical University

Haojie Chen

Shanghai Institute of Nutrition and Health

Yuanjie Niu

Tianjin Medical University

Yong Xu

Nanjing University of Science and Technology

Yangyi Zhang

First Affiliated Hospital of Zhengzhou University

Shuo Wang

Xinjiang Institute of Ecology and Geography

Yong Wang

University of Alabama at Birmingham

Ranlu Liu

Tianjin Medical University General Hospital

Cooperative Institutions

Tianjin Medical University

Second Hospital of Tianjin Medical University

Chinese Academy of Sciences

First Teaching Hospital of Tianjin University of Traditional Chinese Medicine

Sichuan University

Sun Yat-sen University

Nankai University

Tianjin Medical University Cancer Institute and Hospital

Fudan University

University of Chinese Academy of Sciences

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Supplementary Figure from EIF4A3-Induced circARHGAP29 Promotes Aerobic Glycolysis in Docetaxel-Resistant Prostate Cancer through IGF2BP2/c-Myc/LDHA Signaling

Xingkang Jiang Shanqi Guo Shuo Wang Yangyi Zhang Haojie Chen

Supplementary Figure from EIF4A3-Induced circARHGAP29 Promotes Aerobic Glycolysis in Docetaxel-Resistant Prostate Cancer through IGF2BP2/c-Myc/LDHA Signaling

Anaerobic glycolysis

10.1158/0008-5472.22430953

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Supplementary Figure from EIF4A3-Induced circARHGAP29 Promotes Aerobic Glycolysis in Docetaxel-Resistant Prostate Cancer through IGF2BP2/c-Myc/LDHA Signaling

Xingkang Jiang Shanqi Guo Shuo Wang Yangyi Zhang Haojie Chen

Supplementary Figure from EIF4A3-Induced circARHGAP29 Promotes Aerobic Glycolysis in Docetaxel-Resistant Prostate Cancer through IGF2BP2/c-Myc/LDHA Signaling

Anaerobic glycolysis

10.1158/0008-5472.22430947

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Supplementary Figures 1 and 2 from Exosomal lincROR Promotes Docetaxel Resistance in Prostate Cancer through a β-catenin/HIF1α Positive Feedback Loop

Xingkang Jiang Yong Xu Ranlu Liu Shanqi Guo

S1. A. CCK-8 assay was used to detect the cytotoxicity of DTX in DTX-resistant PCa cells (PC3/DR and DU145/DR) and their parental sensitive cells (PC3 and DU145). B. The list of hypoxia-related lncRNAs from Pubmed and the top 80 upregulated lncRNAs in PC3/DR cells from RNA-seq (Jiang X, et al. Front Oncol, 2022). The data are presented as the mean ± S.D. of at least three independent experiments. *P < 0.05.S2. A. The relative expression of lincROR was evaluated by qRT-PCR in PC3 and DU145 cells after being transfected with lincROR. B. DU145 cells were treated with different dosages of DTX (concentration of 0, 5, 10, 20, 40, and 80 nM) for 72 hours and cell viability was evaluated by a CCK-8 assay. C. The LDH release in the culture medium was detected in lincROR-transfected DU145 cells after DTX treatment. D. The expression of lincROR was evaluated in PC3/DR and DU145/DR cells after transfected with siROR #1 or #2. E. The cytotoxicity of DTX in DU145/DR cells was detected by CCK-8 assay after lincROR knockdown. F. The LDH release in culture medium was detected in lincROR-knockdown DU145/DR cells after DTX treatment. The data are presented as the mean ± S.D. of at least three independent experiments.

DU145

Viability assay

10.1158/1541-7786.22725098.v1

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Data from Exosomal lincROR Promotes Docetaxel Resistance in Prostate Cancer through a β-catenin/HIF1α Positive Feedback Loop

Xingkang Jiang Yong Xu Ranlu Liu Shanqi Guo

<div>AbstractEmerging evidence has suggested that patients with metastatic prostate cancer will become resistant after receiving docetaxel (DTX) chemotherapy, but the specific regulatory mechanism is still unclear. lincROR is an important oncogenic long noncoding RNA which plays an important role in regulating tumor carcinogenesis and metastasis; however, the underlying mechanism of lincROR functioning in the DTX resistance process of prostate cancer remains largely unknown. In the current study, we found that lincROR is highly expressed in DTX-resistant prostate cancer cell lines and was associated with poor DTX response in patients with metastatic prostate cancer. By using loss- and gain-of-function experiments revealed that lincROR promotes prostate cancer cells growth and DTX resistance in vitro and in vivo. Mechanistic studies demonstrated that lincROR specifically interacts with and stabilizes MYH9 protein, which enhances β-catenin/hypoxia-inducible factor 1-alpha (HIF1α) pathways. Besides, HIF1α could bind with the promoter region of lincROR to activate its transcription, thus forming the lincROR/MYH9/HIF1α positive feedback loop. Moreover, lincROR could be packaged into exosomes in an heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1)-dependent manner and then disseminated chemoresistance phenotype to receipt cells. Overall, our study provides evidence supporting exosome-mediated lincROR activates the β-catenin/HIF1α positive feedback loop by targeting MYH9 protein, which may be exploited for anticancer therapy.Implications:Our findings suggest that targeting hypoxia stress and chemoresistance for therapeutic purposes and lincROR could promote the improvement of treatment responses in patients with DTX-resistant prostate cancer.</div>

Exosome

10.1158/1541-7786.c.6545826.v2

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Data from EIF4A3-Induced circARHGAP29 Promotes Aerobic Glycolysis in Docetaxel-Resistant Prostate Cancer through IGF2BP2/c-Myc/LDHA Signaling

Xingkang Jiang Shanqi Guo Shuo Wang Yangyi Zhang Haojie Chen

<div>AbstractDocetaxel-based chemotherapy is a standard-of-care treatment for metastatic prostate cancer, and chemoresistance remains a major challenge in clinical practice. Recent studies have demonstrated that circular RNAs (circRNA) play critical roles in the development and progression of prostate cancer. However, the biological roles and potential functions of circRNAs in mediating docetaxel-resistant prostate cancer have yet to be well elucidated. In this study, we analyzed the expression profiles of circRNAs in docetaxel-resistant and -sensitive prostate cancer cells through RNA sequencing and found that expression of circARHGAP29 was significantly upregulated in docetaxel-resistant cell lines and clinical samples. Ectopic expression of circARHGAP29 triggered docetaxel resistance and aerobic glycolysis in prostate cancer cells, which was reduced by silencing circARHGAP29. Moreover, eukaryotic initiation factor 4A3, which bound the back-spliced junction site and the downstream flanking sequence of circARHGAP29, induced cyclization and cytoplasmic export of circARHGAP29. circARHGAP29 increased the stability of lactate dehydrogenase A (LDHA) mRNA by strengthening its interaction with insulin-like growth factor 2 mRNA-binding protein 2, leading to enhanced glycolytic metabolism. In addition, circARHGAP29 interacted with and stabilized c-Myc mRNA and protein, which further increased LDHA expression by facilitating its transcription. These findings reveal the crucial function of circARHGAP29 in prostate cancer glycolysis by increasing and stabilizing LDHA mRNA, providing a promising therapeutic target in docetaxel-resistant prostate cancer.Significance:Upregulation of a novel circRNA, circARHGAP29, promotes docetaxel resistance and glycolytic metabolism, suggesting it could be a prognostic biomarker and therapeutic target in chemoresistant prostate cancer.</div>

Lactate dehydrogenase A

Anaerobic glycolysis

10.1158/0008-5472.c.6513754.v1

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The protective role of Nrf2-Gadd45b against antimony-induced oxidative stress and apoptosis in HEK293 cells

Toxicology Letters (2016)

Xingkang Jiang Zesheng An Chao Lü Yue Chen E Du

HEK 293 cells

10.1016/j.toxlet.2016.05.016

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PTCSC1 Promotes Bladder Cancer Progression by AKT Pathway

Research Square (Research Square) (2021)

Xingkang Jiang shaokun ren Zheng Zhang Wei Zhang

Abstract In bladder cancer the expression of PTCSC1is elevated, but how PTCSC1influencetumor progression are still unclear. We found that in human bladder cancer PTCSC1 is upregulated. The study showedthat the expression level of PTCSC1 is higher in bladder cancer tissuesthan that of PTCSC1 in para-carcinoma tissue. Furthermore, PTCSC1promoted bladder cancer cell migration and invasion, and decreased expression of PTCSC1 inhibited the expression of matrix metalloprotease MMP2and MMP9, and increased the expression level of E-cadherin. PTCSC1 promoted tumor growth in a mouse model of human bladder cancer. Additionally,PTCSC1 shRNA caused a significant decrease in p-AKTexpression in T24 cells and BIU-87 cells, but the overexpression ofPTCSC1got an opposite result.Allthe results showed that PTCSC1 can influencebladder cancer cellmigration and invasion ability by the AKT pathways. PTCSC1 may be an effective therapeutic target in bladder cancer.

MMP9

10.21203/rs.3.rs-626440/v1

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Development and Validation of Newly Biopsy-Free Nomograms for Predicting Clinically Significant Prostate Cancer in Men with PI-RADS ≥4 Lesions

Research Square (Research Square) (2024)

Junxin Wang Mingzhe Chen Yong Xu Shanqi Guo Xingkang Jiang

Abstract To develop and validate biopsy-free nomograms to more accurately predict clinically significant prostate cancer (csPCa) in biopsy-naïve men with Prostate Imaging Reporting and Data System (PI-RADS) ≥ 4 lesions. A cohort of 931 patients with PI-RADS ≥ 4 lesions, undergoing prostate biopsies or radical prostatectomy from January 2020 to August 2023, was analyzed. Various clinical variables, including age, prostate-specific antigen (PSA) levels, prostate volume (PV), PSA density (PSAD), prostate health index (PHI), and maximum standardized uptake values (SUVmax) from PSMA PET-CT imaging, were assessed for predicting csPCa. Model performance was evaluated using area under the receiver operating characteristic curve (AUC), calibration plots, and decision-curve analyses, with internal validation. The foundational model (nomogram 1) encompassed the entire cohort, accurately predicting csPCa by incorporating variables such as age, PSAD, PV, PSA ratio variations, suspicious lesion location, and history of acute urinary retention (AUR). The AUC for csPCa prediction achieved by the foundational model was 0.918, with internal validation confirming reliability (AUC: 0.908). Advanced models (nomogram 2 and 3), incorporating PHI and PHI + PSMA SUVmax, achieved AUCs of 0.908 and 0.955 in the training set and 0.847 and 0.949 in the validation set, respectively. Decision analysis indicated enhanced biopsy outcome predictions with the advanced models. Nomogram 3 could potentially reduce biopsies by 92.41%, while missing only 1.53% of csPCa cases. In conclusion, the newly biopsy-free approaches for patients with PI-RADS ≥ 4 lesions represent a significant advancement in csPCa diagnosis in this high-risk population.

Nomogram

10.21203/rs.3.rs-4695012/v1

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Data from EIF4A3-Induced circARHGAP29 Promotes Aerobic Glycolysis in Docetaxel-Resistant Prostate Cancer through IGF2BP2/c-Myc/LDHA Signaling

Xingkang Jiang Shanqi Guo Shuo Wang Yangyi Zhang Haojie Chen

Anaerobic glycolysis

Protist

10.1158/0008-5472.c.6513754

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Genetic and epigenetic silencing of mircoRNA-506-3p enhances COTL1 oncogene expression to foster non-small lung cancer progression

Oncotarget (2016)

Shanqi Guo Peiying Yang Xingkang Jiang Xiaojiang Li Yuanyuan Wang

Although previous studies suggested that microRNA-506-3p (miR-506-3p) was frequently downregulated, and functioned as a tumor suppressor in several cancers, the biological role and intrinsic regulatory mechanisms of miR-506-3p in non-small cell lung cancer (NSCLC) remain elusive. The present study found miR-506-3p expression was downregulated in advanced NSCLC tissues and cell lines. The expression of miR-506-3p in NSCLC was inversely correlated with larger tumor size, advanced TNM stage and lymph node metastasis. In addition, we also found patients with lower expression of miR-506-3p had a poor prognosis than those patients with higher expression of miR-506-3p. Function studies demonstrated that aberrant miR-506-3p expression modulates tumor cell growth, cell mobility, cell migration and invasion in vitro and in vivo. Mechanistic investigations manifested that coactosin-like protein 1 (COTL1) was a direct downstream target of miR-506-3p. Knockdown of COTL1 mimicked the tumor-suppressive effects of miR-506-3p overexpression in A549 cells, whereas COTL1 overexpression enhanced the tumorigenic function in HCC827 cells. Importantly, we also found GATA3 transcriptionally actives miR-506-3p expression, and the long non-coding RNA urothelial carcinoma-associated 1 (UCA1) exerts oncogenic function in NSCLC by competitively 'sponging' miRNA-506. Together, our combined results elucidated genetic and epigenetic silencing of miR-506-3p enhances COTL1 oncogene expression to foster NSCLC progression.

Tumor progression

10.18632/oncotarget.13501

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