Research Papers:

Suppression of PC-1/PrLZ sensitizes prostate cancer cells to ionizing radiation by attenuating DNA damage repair and inducing autophagic cell death

Zeng-Fu Shang, Qiang Wei, Lan Yu, Fang Huang, Bei-Bei Xiao, Hongtao Wang, Man Song, Li Wang, Jianguang Zhou, Jian Wang and Shanhu Li _

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Oncotarget. 2016; 7:62340-62351. https://doi.org/10.18632/oncotarget.11470

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Zeng-Fu Shang1,*, Qiang Wei3,*, Lan Yu2,*, Fang Huang2, Bei-Bei Xiao1, Hongtao Wang2, Man Song1, Li Wang2, Jianguang Zhou2, Jian Wang2, Shanhu Li2

1School of Radiation Medicine and Protection, Medical College of Soochow University, Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Suzhou, Jiangsu 215123, China

2Laboratory of Medical Molecular Biology, Beijing Institute of Biotechnology, Beijing 100850, China

3Department of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, 510515, China

*These authors have contributed equally to this work

Correspondence to:

Shanhu Li, email: [email protected]

Jian Wang, email: [email protected]

Keywords: PC-1/PrLZ, PCa, autophage, radiotherapy

Received: February 6, 2016    Accepted: August 09, 2016    Published: August 22, 2016


Radiotherapy is promising and effective for treating prostate cancer but the addition of a tumor cell radiosensitizer would improve therapeutic outcomes. PC-1/PrLZ, a TPD52 protein family member is frequently upregulated in advanced prostate cancer cells and may be a biomarker of aggressive prostate cancer. Therefore, we investigated the potential role of PC-1/PrLZ for increasing radioresistance in human prostate cancer cell lines. Growth curves and survival assays after g-ray irradiation confirmed that depletion of endogenous PC-1/PrLZ significantly increased prostate cancer cell radiosensitivity. Irradiation (IR) increased PC-1/PrLZ expression in a dose- and time-dependent manner and increased radiosensitivity in PC-1/PrLZ-suppressed cells was partially due to decreased DNA double strand break (DBS) repair which was measured with comet and gH2AX foci assays. Furthermore, depletion of PC-1/PrLZ impaired the IR-induced G2/M checkpoint, which has been reported to be correlate with radioresistance in cancer cells. PC-1/PrLZ-deficient cells exhibited higher level of autophagy when compared with control cells. Thus, specific inhibition of PC-1/PrLZ might provide a novel therapeutic strategy for radiosensitizing prostate cancer cells.

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