17β-Estradiol Through Activating G Protein-Coupled Estrogen Receptor Exacerbated the Complication of Benign Prostate Hyperplasia in Type 2 Diabetes Mellitus by Inducing Prostatic Proliferation DOI
Tingting Yang,

Zhen Qiu,

YuTian He

et al.

Published: Jan. 1, 2023

Background: Benign prostate hyperplasia (BPH) was one of the major chronic complications type 2 diabetes mellitus (T2DM), and sex steroid hormones were common risk factors for occurrence T2DM BPH.Methods: The profiles simultaneous quantified by LC-MS/MS in clinical serum patients, including simple BPH, new diagnosed T2DM, complicated with BPH matched healthy subjects. Clinical tissues, G protein-coupled estrogen receptor (GPER) inhibitor G15, GPER knockdown lentivirus, YAP1 Verteporfin, knockdown/overexpression targeted metabolomics analysis, Co-IP assays used to investigate molecular mechanisms dysregulated pathological process BPH.Findings: Along prostatic epithelial cells (PECs) proliferation, patients. Sex hormone metabolic patients had greatest degree separation from that As contributor hormones, elevated 17β-estradiol (E2) a significant positive relationship characteristics BPH. E2 through activating exacerbated high glucose (HG)-induced PECs proliferation formation YAP1-TEAD4 heterodimer via Hippo signaling. Knockdown or inhibition GPER-mediated Hippo-YAP1 signaling suppressed HG co-cultured BPH-1 cells. anti-proliferative effects verteporfin, an YAP1, blocked overexpression cells.Interpretation: Inactivating E2/GPER/Hippo/YAP1 might be effective delaying progression inhibiting proliferation.Clinical Trial Registration Details: This study registered Chinese Register (No. ChiCTR1800020339).Funding Information: work supported National Natural Science Foundation China (81973377, 81903689, 82073906 82273987), Key Jiangsu Higher Education Institutions (19KJA460008 19KJB350006), Priority Academic Program Development (PAPD), initializing Fund Xuzhou Medical University (D2018011), Postgraduate Research Practice Innovation Province (KYCX22-2966 KYCX23-2967). Declaration Interests: authors declare no competing interests. Ethics Approval Statement: All procedures studies performed according Helsinki. approved Committee Affiliated Hospital XYFY2018-KL093).

Language: Английский

17β-Estradiol, through activating the G protein-coupled estrogen receptor, exacerbates the complication of benign prostatic hyperplasia in type 2 diabetes mellitus patients by inducing prostate proliferation DOI Creative Commons
Tingting Yang,

Zhen Qiu,

Jiaming Shen

et al.

Journal of Pharmaceutical Analysis, Journal Year: 2024, Volume and Issue: 14(9), P. 100962 - 100962

Published: March 12, 2024

Benign prostatic hyperplasia (BPH) is one of the major chronic complications type 2 diabetes mellitus (T2DM), and sex steroid hormones are common risk factors for occurrence T2DM BPH. The profiles simultaneously quantified by LC-MS/MS in clinical serum patients, including simple BPH newly diagnosed complicated with patients matched healthy individuals. G protein-coupled estrogen receptor (GPER) inhibitor G15, GPER knockdown lentivirus, YAP1 verteporfin, knockdown/overexpression targeted metabolomics analysis, Co-IP assays used to investigate molecular mechanisms disrupted homeostasis pathological process hormone accompanying proliferated epithelial cells (PECs). metabolic have greatest degrees separation from those Elevated 17β-estradiol (E2) key contributor homeostasis, significantly positively related characteristics Activating E2 via Hippo-YAP1 signaling exacerbates high glucose (HG)-induced PECs proliferation through formation YAP1-TEAD4 heterodimer. Knockdown or inhibition GPER-mediated suppresses HG co-treated BPH-1 cells. anti-proliferative effects an YAP1, blocked overexpression Inactivating E2/GPER/Hippo/YAP1 may be effective at delaying progression inhibiting proliferation.

Language: Английский

Citations

1
Hippo signaling modulation and its biological implications in urological malignancies DOI
Tongyu Tong,

Mengjun Huang,

Binyuan Yan

et al.

Molecular Aspects of Medicine, Journal Year: 2024, Volume and Issue: 98, P. 101280 - 101280

Published: June 12, 2024

Language: Английский

Citations

1
Molecular mechanisms of ferroptosis and its effects on bladder cancer. DOI
Ruijie Li,

Yiping Ning,

Yacheng Yuan

et al.

PubMed, Journal Year: 2024, Volume and Issue: 49(2), P. 286 - 295

Published: Feb. 28, 2024

Bladder cancer (BC) is one of the 3 common malignant tumors in urinary system, with high incidence, easy metastasis, poor therapeutic efficacy, and prognosis, which seriously threatens health human. Tumor cells exhibit a strong demand for iron, iron overload can induce ferroptosis, an dependent cell death caused by lipid peroxidation membrane damage. Therefore, ferroptosis has anti-tumor potential. The molecular mechanisms associated abnormalities cellular phospholipid metabolism metabolism, dysregulation antioxidant non-antioxidant systems Xc

Language: Английский

Citations

0
Transcriptomic profiling and risk assessment in bladder cancer: Insights from copper death-related genes DOI
Xu Wang, Long Jin, Xiaoyu Zhang

et al.

Cellular Signalling, Journal Year: 2024, Volume and Issue: 121, P. 111237 - 111237

Published: May 27, 2024

Language: Английский

Citations

0
Advances in research on the carcinogenic mechanisms and therapeutic potential of YAP1 in bladder cancer (Review) DOI Creative Commons

Tianyu Huang,

L. Fan, Jiajia Tang

et al.

Oncology Reports, Journal Year: 2024, Volume and Issue: 53(1)

Published: Nov. 12, 2024

Bladder cancer is the most common malignant tumor of urinary system with high morbidity and no clear pathogenesis. The Hippo signaling pathway an evolutionarily conserved that regulates organ size maintains tissue homeostasis. Yes‑associated protein 1 (YAP1) a key effector this downstream target genes by binding to transcriptional co‑activators PDZ sequences (TAZ). Several studies have demonstrated YAP1 overexpressed in bladder involved adverse outcomes such as occurrence, progression, resistance cisplatin recurrence tumours. present review summarized involvement disease onset mechanism treatment. In addition, study further explored potential diagnosis treatment cancer. This aimed explore

Language: Английский

Citations

0
Polyphyllin II suppresses cell migration, invasion, and metastasis by inducing cytoskeletal rearrangement through the ROCK1/LIMK/CFL1 pathway in bladder cancer cells DOI Creative Commons
Zhiyong Liu, Zhonghua Sun, Yuning Xie

et al.

Acta Materia Medica, Journal Year: 2024, Volume and Issue: 3(4)

Published: Jan. 1, 2024

This study was aimed at determining the antimetastatic effect of polyphyllin II (PPII) in bladder cancer (BC) and underlying mechanisms vitro vivo . Wound healing, Transwell assays, phalloidin staining were performed to determine effects PPII on BC cell migration, invasion, cytoskeletal formation. Gene transcription expression changes detected via RNA sequencing western blotting. The subchronic toxicity evaluated Nu/Nu nude mice. inhibited migration invasion cells. Bioinformatics analysis indicated that regulation a potentially regulated process. restrained formation, as confirmed by staining. Mechanistically, found decrease p-LIMK1/2 p-CFL1 through ROCK1, inhibit increased levels abilities cells induced constitutively active RHOA. Subchronic evaluation revealed 3.0 mg/kg had limited tissue morphology, alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase. Furthermore, treatment effectively formation pulmonary metastatic nodules, well p-LIMK1, lungs. Thus, inhibits metastasis RHOA-ROCK1-LIMK1/2-CFL1 axis, is potential candidate for drug development.

Language: Английский

Citations

0
Preliminary study on the cellular and molecular mechanisms of Cms1 ribosomal small subunit homolog promoting hepatocellular carcinoma progression via activation of the homolog family member A/yes-associated protein 1 signaling pathway DOI Open Access

Yao Zheng,

Aiyun Wang, Shiying Yu

et al.

CytoJournal, Journal Year: 2024, Volume and Issue: 21, P. 61 - 61

Published: Dec. 11, 2024

The precise mechanism of action cms1 ribosomal small subunit homolog (CMSS1) in hepatocellular carcinoma (HCC) is yet unknown, although it may be essential to the malignant evolution disease. aim this study was reveal role CMSS1 HCC and its possible mechanism. expression different cell lines detected by quantitative real-time polymerase chain reaction Western blot. cells subsequently silenced, proliferation capacity measured colony formation assay, 5-ethynyl-2'-deoxyuridine (EdU) flow cytometry, migration metastasis Transwell assay Finally, ras family member A (RhoA) yes-associated protein 1 (YAP1) were relationship between CMSS1, RhoA, YAP1 further discussed immunofluorescence, EdU assay. experimental results showed that highly expressed tissues (P < 0.001). Further experiments demonstrated promotes progression activating RhoA GTPase/YAP1 signaling pathway Inhibition could reverse enhanced ability induced Silencing can inhibit epithelial- mesenchymal transition 0.01). Moreover, silencing reduces nuclear translocation pathway.

Language: Английский

Citations

0
The Expression Regulation and Cancer-Promoting Roles of RACGAP1 DOI Creative Commons
Jiacheng Lin,

Yuhao Zhu,

Zhaoping Lin

et al.

Biomolecules, Journal Year: 2024, Volume and Issue: 15(1), P. 3 - 3

Published: Dec. 24, 2024

RACGAP1 is a Rho-GTPase-activating protein originally discovered in male germ cells to inactivate Rac, RhoA and Cdc42 from the GTP-bound form GDP-bound form. GAP has traditionally been known as tumor suppressor. However, studies increasingly suggest that overexpressed activates Rac multiple cancers mediate downstream oncogene overexpression by assisting nuclear translocation of signaling molecules promote cytokinesis regulating cytoskeleton or serving component central spindle. Contradictorily, it was also reported gastric cancer could RhoA. In addition, have revealed can be biomarker for prognosis, its role reducing doxorubicin sensitivity poses difficulties treatment, while current drug targets mainly focus on molecule. This article reviews expression regulation cancer-promoting functions through mediation Rho-GTPase activation.

Language: Английский

Citations

0
17β-Estradiol Through Activating G Protein-Coupled Estrogen Receptor Exacerbated the Complication of Benign Prostate Hyperplasia in Type 2 Diabetes Mellitus by Inducing Prostatic Proliferation DOI
Tingting Yang,

Zhen Qiu,

YuTian He

et al.

Published: Jan. 1, 2023

Background: Benign prostate hyperplasia (BPH) was one of the major chronic complications type 2 diabetes mellitus (T2DM), and sex steroid hormones were common risk factors for occurrence T2DM BPH.Methods: The profiles simultaneous quantified by LC-MS/MS in clinical serum patients, including simple BPH, new diagnosed T2DM, complicated with BPH matched healthy subjects. Clinical tissues, G protein-coupled estrogen receptor (GPER) inhibitor G15, GPER knockdown lentivirus, YAP1 Verteporfin, knockdown/overexpression targeted metabolomics analysis, Co-IP assays used to investigate molecular mechanisms dysregulated pathological process BPH.Findings: Along prostatic epithelial cells (PECs) proliferation, patients. Sex hormone metabolic patients had greatest degree separation from that As contributor hormones, elevated 17β-estradiol (E2) a significant positive relationship characteristics BPH. E2 through activating exacerbated high glucose (HG)-induced PECs proliferation formation YAP1-TEAD4 heterodimer via Hippo signaling. Knockdown or inhibition GPER-mediated Hippo-YAP1 signaling suppressed HG co-cultured BPH-1 cells. anti-proliferative effects verteporfin, an YAP1, blocked overexpression cells.Interpretation: Inactivating E2/GPER/Hippo/YAP1 might be effective delaying progression inhibiting proliferation.Clinical Trial Registration Details: This study registered Chinese Register (No. ChiCTR1800020339).Funding Information: work supported National Natural Science Foundation China (81973377, 81903689, 82073906 82273987), Key Jiangsu Higher Education Institutions (19KJA460008 19KJB350006), Priority Academic Program Development (PAPD), initializing Fund Xuzhou Medical University (D2018011), Postgraduate Research Practice Innovation Province (KYCX22-2966 KYCX23-2967). Declaration Interests: authors declare no competing interests. Ethics Approval Statement: All procedures studies performed according Helsinki. approved Committee Affiliated Hospital XYFY2018-KL093).

Language: Английский

Citations

0