Keywords

microRNA, let-7, lung cancer, non-coding RNA

Presentation Type

Poster

Research Abstract

MicroRNAs (miRNAs) are small, noncoding RNAs that regulate protein levels typically by interacting with the 3′ untranslated region (3′-UTR) of target messenger RNA (mRNAs) and are often aberrantly expressed in cancer. The let-7 miRNA family members are commonly regarded as cancer suppressors, by down-regulating the expression of oncoproteins such as RAS, HMGA2, and MYC. However, prior work indicates that unprocessed let-7 RNAs may be positively correlated with cancer phenotypes in lung cancer cell lines. Our study aims to identify the effects of unprocessed let-7a-1 and let-7a-3 in non-small cell lung cancer, by transfecting plasmids that express unprocessed let-7a-1 and let-7a-3 into 3 different lung cancer cell lines. We then proceeded to conduct functional assays to measure the differences in anchorage independent growth, cell proliferation, and cell migration in all cell lines transfected with unprocessed let-7, in contrast to cells transfected with a control vector and thus far determined that unprocessed let-7a-1 can enhance anchorage independent growth. Thus, we created truncations of the let-7a-1 miRNA to identify the cis regions of this miRNA that is responsible for the change in phenotype. Our results suggest that cells transfected with truncated, yet unprocessed let-7a-1 have increased anchorage independent growth, a major hallmark of cancer cell. There is still a need to replicate the functional assays that were conducted while continuing to create constructs of both let-7a-1 and let-7a-3 in order to further identify the sequence of the miRNAs responsible for the enhanced cancer phenotypes.

Session Track

Health

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Aug 4th, 12:00 AM

Identifying the Effects of Unprocessed let-7a-1 and let-7a-3 in Non-Small Cell Lung Cancer

MicroRNAs (miRNAs) are small, noncoding RNAs that regulate protein levels typically by interacting with the 3′ untranslated region (3′-UTR) of target messenger RNA (mRNAs) and are often aberrantly expressed in cancer. The let-7 miRNA family members are commonly regarded as cancer suppressors, by down-regulating the expression of oncoproteins such as RAS, HMGA2, and MYC. However, prior work indicates that unprocessed let-7 RNAs may be positively correlated with cancer phenotypes in lung cancer cell lines. Our study aims to identify the effects of unprocessed let-7a-1 and let-7a-3 in non-small cell lung cancer, by transfecting plasmids that express unprocessed let-7a-1 and let-7a-3 into 3 different lung cancer cell lines. We then proceeded to conduct functional assays to measure the differences in anchorage independent growth, cell proliferation, and cell migration in all cell lines transfected with unprocessed let-7, in contrast to cells transfected with a control vector and thus far determined that unprocessed let-7a-1 can enhance anchorage independent growth. Thus, we created truncations of the let-7a-1 miRNA to identify the cis regions of this miRNA that is responsible for the change in phenotype. Our results suggest that cells transfected with truncated, yet unprocessed let-7a-1 have increased anchorage independent growth, a major hallmark of cancer cell. There is still a need to replicate the functional assays that were conducted while continuing to create constructs of both let-7a-1 and let-7a-3 in order to further identify the sequence of the miRNAs responsible for the enhanced cancer phenotypes.