{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T17:25:57Z","timestamp":1790357157645,"version":"4.1.0"},"reference-count":51,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2020,11,13]],"date-time":"2020-11-13T00:00:00Z","timestamp":1605225600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"Biomedical and Graduate Research Organization of Georgetown University Medical Center"},{"name":"King Saud bin Abdulaziz University for Health Sciences"},{"name":"Government of Saudi Arabia"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,4,17]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Despite impressive advances in the treatment of prostate cancer with various efficacious inhibitors along the androgen\/androgen receptor axis, eventual development of incurable metastatic Castration-Resistant Prostate Cancer (mCRPC) is inevitable and remains a major clinical challenge. Constitutively active androgen receptor (AR) spliced variants have emerged as primary means of resistance to anti-androgens and androgen synthesis inhibitors. The alternatively spliced AR variant, ARv7, has attracted significant interest due to its constitutively active status in CRPC that drives androgen-independence. Factors that are involved in regulating ARv7 levels in CRPC are not clearly known. We recently demonstrated that a protein kinase, T-LAK cell-originated protein kinase (TOPK) level correlates with the aggressiveness of prostate cancer and its invasive behavior. In this study, we investigated whether TOPK plays a role in driving androgen-independence in prostate cancer cells. Our data demonstrate that TOPK overexpression in androgen-dependent LNCaP and VCaP induces ARv7 and drives androgen-independent growth. On the other hand, pharmacological inhibition of TOPK in androgen-independent LNCaP95 and 22Rv1 represses AR transactivation, and AR stability. In summary, this study illustrates a direct role of TOPK in regulating ARv7 and driving androgen-independence in prostate cancer cells.<\/jats:p>","DOI":"10.1093\/carcin\/bgaa120","type":"journal-article","created":{"date-parts":[[2020,11,7]],"date-time":"2020-11-07T20:10:21Z","timestamp":1604779821000},"page":"423-435","source":"Crossref","is-referenced-by-count":7,"title":["T-LAK cell-originated protein kinase (TOPK) enhances androgen receptor splice variant (ARv7) and drives androgen-independent growth in prostate cancer"],"prefix":"10.1093","volume":"42","author":[{"given":"Lama","family":"Alhawas","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karishma S","family":"Amin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bharath","family":"Salla","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Partha P","family":"Banerjee","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular & Cellular Biology, Georgetown University Medical Center, Washington, DC, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2020,11,13]]},"reference":[{"key":"2021041713561783900_CIT0001","first-page":"293","article-title":"Studies on prostatic cancer i. the effect of castration, of estrogen and of androgen injection on serum phosphatases in metastatic carcinoma of the prostate","volume":"1","author":"Charles","year":"1941","journal-title":"Cancer Res"},{"key":"2021041713561783900_CIT0002","doi-asserted-by":"crossref","first-page":"1335","DOI":"10.1158\/1078-0432.CCR-12-2910","article-title":"Enzalutamide: a novel antiandrogen for patients with castrate-resistant prostate cancer","volume":"19","author":"Jean","year":"2013","journal-title":"Clin. 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