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]
Copyright of International Journal of Radiation Oncology, Biology, Physics is the property of Pergamon Press - An Imprint of Elsevier Science and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Lin28-let7 modulates radiosensitivity of human cancer cells with activation of K-Ras.
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  Data: <searchLink fieldCode="AR" term="%22Oh+JS%22">Oh JS</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Kim+JJ%22">Kim JJ</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Byun+JY%22">Byun JY</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Kim+IA%22">Kim IA</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Oh%2C+Jee-Sun%22">Oh, Jee-Sun</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Kim%2C+Jae-Jin%22">Kim, Jae-Jin</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Byun%2C+Ju-Yeon%22">Byun, Ju-Yeon</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Kim%2C+In-Ah%22">Kim, In-Ah</searchLink> (AUTHOR)
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  Data: <searchLink fieldCode="JN" term="%22International+Journal+of+Radiation+Oncology%2C+Biology%2C+Physics%22">International Journal of Radiation Oncology, Biology, Physics</searchLink>. Jan2010, Vol. 76 Issue 1, p5-8. 4p.
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: <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]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of International Journal of Radiation Oncology, Biology, Physics is the property of Pergamon Press - An Imprint of Elsevier Science and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1016/j.ijrobp.2009.08.028
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              Text: Jan2010
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