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Lin28-let7 modulates radiosensitivity of human cancer cells with activation of K-Ras.

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Title: Lin28-let7 modulates radiosensitivity of human cancer cells with activation of K-Ras.
Authors: Oh JS (AUTHOR), Kim JJ (AUTHOR), Byun JY (AUTHOR), Kim IA (AUTHOR), Oh, Jee-Sun1 (AUTHOR), Kim, Jae-Jin (AUTHOR), Byun, Ju-Yeon (AUTHOR), Kim, In-Ah (AUTHOR)
Source: International Journal of Radiation Oncology, Biology, Physics. Jan2010, Vol. 76 Issue 1, p5-8. 4p.
Abstract: Purpose: To evaluate the potential of targeting Lin28-let7 microRNA regulatory network for overcoming the radioresistance of cancer cells having activated K-Ras signaling.Methods and Materials: A549 lung carcinoma cells and ASPC1 pancreatic cancer cells possessing K-RAS mutation were transfected with pre-let7a microRNA or Lin28 siRNA, respectively. Clonogenic assay, quantitative reverse transcription polymerase chain reaction, and Western analysis were performed. The effects of Lin28 on SQ20B cells having wild-type K-RAS, and a normal fibroblast were also assessed.Results: The overexpression of let-7a decreased expression of K-Ras and radiosensitized A549 cells. Inhibition of Lin28, a repressor of let-7, attenuated K-Ras expression and radiosensitized A549 and ASPC1 cells. Neither SQ20B cells expressing wild-type K-RAS nor HDF, the normal human fibroblasts, were radiosensitized by this approach.Conclusions: The Lin28-let7 regulatory network may be a potentially useful therapeutic target for overcoming the radioresistance of human cancers having activated K-Ras signaling. [ABSTRACT FROM AUTHOR]
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Database: Engineering Source
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Abstract:<bold>Purpose: </bold>To evaluate the potential of targeting Lin28-let7 microRNA regulatory network for overcoming the radioresistance of cancer cells having activated K-Ras signaling.<bold>Methods and Materials: </bold>A549 lung carcinoma cells and ASPC1 pancreatic cancer cells possessing K-RAS mutation were transfected with pre-let7a microRNA or Lin28 siRNA, respectively. Clonogenic assay, quantitative reverse transcription polymerase chain reaction, and Western analysis were performed. The effects of Lin28 on SQ20B cells having wild-type K-RAS, and a normal fibroblast were also assessed.<bold>Results: </bold>The overexpression of let-7a decreased expression of K-Ras and radiosensitized A549 cells. Inhibition of Lin28, a repressor of let-7, attenuated K-Ras expression and radiosensitized A549 and ASPC1 cells. Neither SQ20B cells expressing wild-type K-RAS nor HDF, the normal human fibroblasts, were radiosensitized by this approach.<bold>Conclusions: </bold>The Lin28-let7 regulatory network may be a potentially useful therapeutic target for overcoming the radioresistance of human cancers having activated K-Ras signaling. [ABSTRACT FROM AUTHOR]
ISSN:03603016
DOI:10.1016/j.ijrobp.2009.08.028