ArticleOncology reports2018
βKlotho inhibits androgen/androgen receptor‑associated epithelial‑mesenchymal transition in prostate cancer through inactivation of ERK1/2 signaling.
Article in Oncology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 12 citations in OpenAlex.
- Review
- Exploring the Therapeutic Potential of Triptonide in Salivary Adenoid Cystic Carcinoma: A Comprehensive Approach Involving Network Pharmacology and Experimental Validation.Current pharmaceutical design · 2024Article
- Klotho-beta attenuates Rab8a-mediated exosome regulation and promotes prostate cancer progression.Oncogene · 2023Article
- β-Klotho Promotes the Development of Intrauterine Adhesions via the PI3K/AKT Signaling Pathway.International journal of molecular sciences · 2022Article
- Review
- Hijacking Sexual Immuno-Privilege in GBM-An Immuno-Evasion Strategy.International journal of molecular sciences · 2021Article
- Fibroblast Growth Factor Receptors (FGFRs) and Noncanonical Partners in Cancer Signaling.Cells · 2021Review
- Serum β-klotho is a potential biomarker in the prediction of clinical outcomes among patients with NSCLC.Journal of thoracic disease · 2021Article
- βKlotho, a direct target of miR-206, contributes to the growth of hepatoblastoma through augmenting PI3K/Akt/mTOR signaling.American journal of cancer research · 2021Article
- βKlotho Inhibits Cell Proliferation by Downregulating ELK4 and Predicts Favorable Prognosis in Prostate Cancer.Cancer management and research · 2021Article
- NUMB knockdown enhanced the anti-tumor role of cisplatin on ovarian cancer cells by inhibiting cell proliferation and epithelial-mesenchymal transition.Translational cancer research · 2019Article
- Fibroblast Growth Factor Family in the Progression of Prostate Cancer.Journal of clinical medicine · 2019Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epithelial‑mesenchymal transition (EMT) is reported to have intimate crosstalk with androgen receptor (AR) signaling in prostate cancer (PCa) and is known to be responsible for castration resistance. Fibroblast growth factor/receptor (FGF/FGFR) signaling is also involved in tumor progression and EMT in multiple tissues. Several studies have investigated the role of βKlotho, an FGF/FGFR signaling co‑receptor in tumorigenesis. However, its role in PCa remains unknown. In the present study, the role of androgen in the EMT of PCa cells was examined by western blotting. The expression of βKlotho was examined in prostate cells and PCa tissues by western blotting and immunohistochemistry, respectively. The biological role of βKlotho was revealed by a series of functional in vitro and in vivo studies. We determined that βKlotho expression was significantly decreased in PCa tissues compared with benign prostatic hyperplasia (BPH) tissues, and low βKlotho expression was associated with a high Gleason score of PCa. βKlotho overexpression inhibited the viability, migration, and androgen/AR‑associated EMT of PCa cells through the inactivation of ERK1/2 signaling. Notably, βKlotho overexpression inhibited prostate tumor growth and EMT in vivo. Knockdown of βKlotho produced the opposite effects. In conclusion, βKlotho inhibits EMT and plays a tumor‑suppressive role in PCa, linking FGF/FGFR/βKlotho signaling to the regulation of PCa progression.
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