@article {235,
	title = {Knockdown of cullin 4A inhibits growth and increases chemosensitivity in lung cancer cells.},
	journal = {J Cell Mol Med},
	volume = {20},
	year = {2016},
	month = {2016 Jul},
	pages = {1295-306},
	abstract = {<p>Cullin 4A (Cul4A) has been observed to be overexpressed in various cancers. In this study, the role of Cul4A in the growth and chemosensitivity in lung cancer cells were studied. We showed that Cul4A is overexpressed in lung cancer cells and tissues. Knockdown of the Cul4A expression by shRNA in lung cancer cells resulted in decreased cellular proliferation and growth in lung cancer cells. Increased sensitivity to gemcitabine, a chemotherapy drug, was also noted in those Cul4A knockdown lung cancer cells. Moreover, increased expression of p21, transforming growth factor (TGF)-β inducible early gene-1 (TIEG1) and TGF beta-induced (TGFBI) was observed in lung cancer cells after Cul4A knockdown, which may be partially related to increased chemosensitivity to gemcitabine. G0/G1 cell cycle arrest was also noted after Cul4A knockdown. Notably, decreased tumour growth and increased chemosensitivity to gemcitabine were also noted after Cul4A knockdown in lung cancer xenograft nude mice models. In summary, our study showed that targeting Cul4A with RNAi or other techniques may provide a possible insight to the development of lung cancer therapy in the future.</p>},
	issn = {1582-4934},
	doi = {10.1111/jcmm.12811},
	author = {Hung, Ming-Szu and Chen, I-Chuan and You, Liang and Jablons, David M and Li, Ya-Chin and Jiang-Hua Mao and Xu, Zhidong and Lung, Jr-Hau and Yang, Cheng-Ta and Liu, Shih-Tung}
}
@article {230,
	title = {Knockdown of Cul4A increases chemosensitivity to gemcitabine through upregulation of TGFBI in lung cancer cells.},
	journal = {Oncol Rep},
	volume = {34},
	year = {2015},
	month = {2015 Dec},
	pages = {3187-95},
	abstract = {<p>Cullin 4A (Cul4A) promotes oncogenesis through overexpression and then ubiquitination-mediated proteolysis of tumor suppressors in various types of cancers. Transforming growth factor β-induced (TGFBI) has been implicated as a tumor suppressor, which enhances gemcitabine chemosensitivity in lung cancer cells. The present study aimed to investigate the association of TGFBI and Cul4A and the mechanism by which Cul4A regulates TGFBI. In addition, we also evaluated the therapeutic value of Cul4A RNAi using adenoviral transfection of Cul4A RNAi in nude mouse xenograft models. We observed that knockdown of Cul4A was associated with increased sensitivity to gemcitabine through upregulation of TGFBI in lung cancer cells. Cul4A regulated TGFBI through direct interaction and then ubiquitin-mediated protein degradation. In the nude mouse xenograft models, adenoviral transfection of Cul4A RNAi in combination with gemcitabine chemotherapy inhibited lung cancer tumor growth. As the result, combination of Cul4A RNAi with chemotherapy may provide a new approach to lung cancer treatment.</p>},
	keywords = {Animals, Cell Line, Tumor, Cell Transformation, Neoplastic, Cullin Proteins, Deoxycytidine, Drug Resistance, Neoplasm, Extracellular Matrix Proteins, Gene Expression Regulation, Neoplastic, Gene Knockdown Techniques, Humans, Lung Neoplasms, Mice, Transforming Growth Factor beta, Xenograft Model Antitumor Assays},
	issn = {1791-2431},
	doi = {10.3892/or.2015.4324},
	author = {Hung, Ming-Szu and Chen, I-Chuan and You, Liang and Jablons, David M and Li, Ya-Chin and Jiang-Hua Mao and Xu, Zhidong and Hsieh, Meng-Jer and Lin, Yu-Ching and Yang, Cheng-Ta and Liu, Shin-Tung and Tsai, Ying-Huang}
}
