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首页> 外文期刊>Cancer: A Journal of the American Cancer Society >Krüppel-like factor 4 functions as a tumor suppressor in cervical carcinoma
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Krüppel-like factor 4 functions as a tumor suppressor in cervical carcinoma

机译：Krüppel样因子4在宫颈癌中起抑癌作用

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BACKGROUND: The Krüppel-like factor 4 (KLF4) protein, a zinc finger transcription factor that is highly expressed in epithelial tissues such as the gut and skin, has been implicated in both tumor suppression and progression. However, the role of KLF4 in human cervical carcinoma is still unclear. METHODS: The expression of KLF4 in cervical carcinoma tissues and cervical cancer cell lines was examined with immunohistochemistry and Western blot assay. The effects of KLF4 silencing and overexpression on the cell proliferation, cell viability, and tumor formation of cervical cancer cells were investigated. RESULT: KLF4 protein expression showed a pattern of gradual decrease from normal cervix to cervical carcinoma in situ and then to invasive cervical carcinomas (P .05). Overexpression of KLF4 in SiHa and C33A cells resulted in significantly inhibited cell growth and significantly attenuated tumor formation. Consistently, KLF4 silencing in HeLa cells significantly promoted cell growth and tumor formation. Furthermore, KLF4 overexpression caused cell cycle arrest at the G1/S transition, along with the up-regulated expression of p27 Kip1 protein. Promoter analysis revealed that KLF4 transactivated the expression of p27 Kip1 through the specific motif that is between the nucleotides of -435 and -60 in its promoter. The results from chromatin immunoprecipitation assays demonstrated the physical interaction between KLF4 protein and this specific motif in p27 Kip1 promoter. CONCLUSIONS: KLF4 may function as a tumor suppressor in cervical carcinoma by inhibiting cell growth and tumor formation.
机译：背景：Krüppel样因子4（KLF4）蛋白是一种锌指转录因子，在上皮组织（如肠道和皮肤）中高度表达，与肿瘤抑制和进展有关。但是，KLF4在人宫颈癌中的作用仍不清楚。方法：采用免疫组织化学和Western blot方法检测KLF4在宫颈癌组织和宫颈癌细胞株中的表达。研究了KLF4沉默和过表达对宫颈癌细胞增殖，细胞活力和肿瘤形成的影响。结果：KLF4蛋白表达显示出从正常子宫颈到原位子宫颈癌然后再到浸润性子宫颈癌的逐渐减少的模式（P <.05）。 SiHa和C33A细胞中KLF4的过表达导致细胞生长受到明显抑制，肿瘤形成明显减弱。一致地，HeLa细胞中的KLF4沉默显着促进了细胞生长和肿瘤形成。此外，KLF4的过表达导致细胞周期停滞在G1 / S过渡，以及p27 Kip1蛋白的表达上调。启动子分析显示，KLF4通过其启动子中-435和-60核苷酸之间的特定基序使p27 Kip1的表达反式激活。染色质免疫沉淀试验的结果表明，KLF4蛋白与p27 Kip1启动子中的这一特定基序之间存在物理相互作用。结论：KLF4可能通过抑制细胞生长和肿瘤形成而在宫颈癌中起抑癌作用。

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