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Regulation of rat DOC-2 gene during castration-induced rat ventral prostate degeneration and its growth inhibitory function in human prostatic carcinoma cells

Tseng, Ching-Ping, Ely, Brent D., Li, Yingming, Pong, Rey-Chen, Hsieh, Jer-Tsong·1998·Endocrinology
DOI 10.1210/endo.139.8.6159
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Abstract

Androgen is a mitogen as well as a morphogen for prostatic epithelium. However, the detailed mechanisms of these distinct androgenic actions have not yet been delineated. Therefore, we employed differential display PCR to unveil any potential genes that may be involved in these processes. In this study, we report the isolation and characterization of two alternative splicing forms (p82 and p59) of C9 complementary DNA, the rat homolog of the human deletion of ovarian carcinoma 2 (DOC-2) gene and mouse p96 phosphoprotein, from rat ventral prostate (VP). We found that C9 was up-regulated in rat VP after castration, suggesting that C9 may be regulated by androgen receptor directly or indirectly during prostate degeneration. A similar regulatory pattern was also observed in both the seminal vesicle and dorsolateral prostate, but not in the coagulating gland or other androgen-independent organs. Immunohistochemical analysis of rat VP demonstrated that C9 is detected in the basal epithelia and surrounding stromal cells after prolonged castration. Ribonuclease protection assay and Western blot analysis revealed that p59 is the predominant C9 isoform in rat VP. To unveil the function of C9 in cell growth, we transfected p59 complementary DNA into the C4-2 cells, a derivative of the LNCaP prostatic carcinoma cell line. The p59 stable transfectants exhibited a slower growth rate and an increase in the cell fraction in the G1 phase under our experimental conditions. These data indicate that C9-p59 has growth inhibitory activity for prostatic epithelial cells. Taken together, our results suggest that C9 is up-regulated during prostate degeneration process and may play an active role in the proliferation and differentiation of prostatic epithelium.

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  • To date, Dab2 expression has been reported to be reduced or lost in many additional cancer types, including colon, prostate, esophageal, nasopharyngeal, and head and neck.

    “To date, Dab2 expression has been reported to be reduced or lost in many additional cancer types, including colon (Kleeff et al., 2002), prostate (Tseng et al., 1998), esophageal (Anupam et al., 2006), nasopharyngeal (Tong et al., 2010), and head and neck (Hannigan et al., 2010).”

    From Endocytosis and Physiology: Insights from Disabled-2 Deficient Mice (2016) · cites this paper as Tseng et al., 1998

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Metadata

Authors
Tseng, C.-P., Ely, B. D., Li, Y., Pong, R.-C., & Hsieh, J.-T.
Affiliations
Department of Urology, University of Texas Southwestern Medical Center, Dallas, Texas 75235-9110
Venue
Endocrinology
Publisher
The Endocrine Society
Published
1998-08-01
Volume
139
Issue
8
Pages
3542-3553
ISSN
  • 0013-7227
  • 1945-7170
DOI
10.1210/endo.139.8.6159
Cited by
74
References
0
Language
en

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