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Generation of Prostate Cancer Cell Models of Resistance to the Anti-mitotic Agent Docetaxel

Generation of Prostate Cancer Cell Models of Resistance to the Anti-mitotic Agent Docetaxel

Published on: September 8, 2017

Small ankyrin 1 (sANK1) promotes docetaxel resistance in castration-resistant prostate cancer cells by enhancing

Yang Yang¹, Haixiang Qin¹, Meng Ding¹

¹Department of Urology, Drum Tower Hospital, Medical School of Nanjing University, Institute of Urology, Nanjing University, China.

|December 12, 2022

Abstract:

Docetaxel (DTX) plays an important role in treating advanced prostate cancer (PCa). However, nearly all patients receiving DTX therapy ultimately progress to DTX resistance. How to address DTX resistance in PCa remains a key challenge for all urologists. Small ankyrin 1 (sAnk1) is an integral membrane protein in the endoplasmic reticulum. In the present study, we identified that sAnk1 is upregulated in PCa tissues and is positively associated with DTX therapy resistance in PCa. Further investigation demonstrated that overexpression of sAnk1 can significantly increase the DTX-resistant ability of PCa cells in vitro and in vivo. In addition, overexpression of sAnk1 could enhance oxidative phosphorylation (OXPHOS) levels in PCa cells, which was consistent with the higher OXPHOS levels observed in DTX-resistant PCa cells as compared to DTX-sensitive PCa cells. sAnk1 was also found to interact with polypyrimidine-tract-binding protein (PTBP1), an alternative splicing factor, and suppressed PTBP1-mediated alternative splicing of the pyruvate kinase gene (PKM). Thus, overexpression of sAnk1 decreased the ratio of PKM2/PKM1, enhanced the OXPHOS level, and ultimately promoted the resistance of PCa cells to DTX. In summary, our data suggest that sAnk1 enhances DTX resistance in PCa cells.

Insights

Small ankyrin 1 (sAnk1) protein is upregulated in prostate cancer (PCa) and promotes docetaxel (DTX) resistance by enhancing oxidative phosphorylation. Targeting sAnk1 may overcome DTX resistance in PCa patients.

Area of Science:

Oncology
Molecular Biology
Biochemistry

Background:

Docetaxel (DTX) is crucial for advanced prostate cancer (PCa) treatment.
Therapeutic resistance to DTX is a significant clinical challenge in PCa.
Small ankyrin 1 (sAnk1) is an endoplasmic reticulum membrane protein.

Purpose of the Study:

To investigate the role of sAnk1 in DTX resistance in PCa.
To elucidate the molecular mechanisms by which sAnk1 influences DTX resistance.

Main Methods:

Analysis of sAnk1 expression in PCa tissues.
In vitro and in vivo studies of PCa cells with sAnk1 overexpression.
Assessment of oxidative phosphorylation (OXPHOS) levels.
Investigation of sAnk1 interaction with PTBP1 and its effect on PKM splicing.

Main Results:

sAnk1 is upregulated in PCa and associated with DTX resistance.
Overexpression of sAnk1 enhances DTX resistance in PCa cells.
sAnk1 overexpression increases OXPHOS levels in PCa cells.
sAnk1 suppresses PTBP1-mediated PKM alternative splicing, decreasing PKM2/PKM1 ratio.

Conclusions:

sAnk1 promotes DTX resistance in PCa by enhancing OXPHOS.
sAnk1-mediated suppression of PKM splicing contributes to DTX resistance.
sAnk1 is a potential therapeutic target for overcoming DTX resistance in PCa.

Read full analysis

Keywords:

OXPHOS PTBP1 docetaxel resistance prostate cancer sANK1

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