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Expression of Smad4 in prostate cancer LNCaP and ARCaP cell lines with different metastatic potentials and its significance / 中华男科学杂志
National Journal of Andrology ; (12): 41-44, 2009.
Article in Chinese | WPRIM | ID: wpr-292426
ABSTRACT
<p><b>OBJECTIVE</b>To observe the expression of Smad4, the core of TGF-beta/Smads signal transduction pathway in different prostate cancer cell lines, and explore their molecular mechanism of bone metastatic potential.</p><p><b>METHODS</b>The Millicell polycarbonate filter coated with matrigel was used to confirm the invasive potency of LNCaP and ARCaP cell lines (IF11 and IA8). The expressions of the Smad4 protein and mRNA in these prostate cancer cells with different metastatic potentials were detected by Western blotting and RT-PCR, respectively.</p><p><b>RESULTS</b>ARCaP cell lines (IF11 and IA8) exhibited a stronger potency of invasion than LNCaP (P < 0.01). The Smad4 protein and mRNA highly expressed in the LNCaP cell line that was well-known with a low metastatic potential, but not in the ARCaP (IF11 or IA8) cells with high metastatic potentials (P < 0.01).</p><p><b>CONCLUSION</b>Smad4 expresses differently in LNCaP and ARCaP cell lines with different metastatic potentials and, as a tumor suppressive gene, its deficient expression may play an important role in the invasion and metastasis of advanced prostate cancer.</p>
Subject(s)
Full text: Available Index: WPRIM (Western Pacific) Main subject: Pathology / Prostatic Neoplasms / RNA, Messenger / Transforming Growth Factor beta / Cell Line, Tumor / Smad4 Protein / Genetics / Metabolism / Neoplasm Metastasis Limits: Humans / Male Language: Chinese Journal: National Journal of Andrology Year: 2009 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Main subject: Pathology / Prostatic Neoplasms / RNA, Messenger / Transforming Growth Factor beta / Cell Line, Tumor / Smad4 Protein / Genetics / Metabolism / Neoplasm Metastasis Limits: Humans / Male Language: Chinese Journal: National Journal of Andrology Year: 2009 Type: Article