Faculty Mentor

Dr. Yong Teng

Proposal Type

Poster

Start Date

3-11-2018 3:20 PM

End Date

3-11-2018 4:30 PM

Location

Nesbitt 3110

Abstract

Abstract

Breast cancer is the leading malignancy and leading cause of cancer-related death in women globally. The greatest barrier to a treatment is the incomplete understanding of mechanisms underlying molecular regulators whose function is cellular adaptation to estrogen. One such enzyme, ATAD3A, a nuclear-encoded mitochondrial enzyme, has been brought under this lab’s scrutiny. The role of ATAD3A in breast cancer progression is largely unknown but it has been shown to be a crucial mediator in promoting cell cycle progression. The two objectives of this project were: to determine whether the ATAd3A is an Estrogen Receptor-α target (ERα) and to determine the role of (ERα) in estrogen induced ATAD3A upregulation. To test these objectives, four breast cancer cell lines, two or which were ERα+ and two were ERα- were used. ERα knockdown cells were achieved by small interfering RNA. All cell lines were treated to undergo induction of ER activation. Gene expression was determined by real time RT-PCR, western blots, and MTT assays. The results found were statistically significant and pave the way to future experiments.

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Nov 3rd, 3:20 PM Nov 3rd, 4:30 PM

31 - The critical role of ATAD3A in the estrogen signaling pathway in breast cancer cells

Nesbitt 3110

Abstract

Breast cancer is the leading malignancy and leading cause of cancer-related death in women globally. The greatest barrier to a treatment is the incomplete understanding of mechanisms underlying molecular regulators whose function is cellular adaptation to estrogen. One such enzyme, ATAD3A, a nuclear-encoded mitochondrial enzyme, has been brought under this lab’s scrutiny. The role of ATAD3A in breast cancer progression is largely unknown but it has been shown to be a crucial mediator in promoting cell cycle progression. The two objectives of this project were: to determine whether the ATAd3A is an Estrogen Receptor-α target (ERα) and to determine the role of (ERα) in estrogen induced ATAD3A upregulation. To test these objectives, four breast cancer cell lines, two or which were ERα+ and two were ERα- were used. ERα knockdown cells were achieved by small interfering RNA. All cell lines were treated to undergo induction of ER activation. Gene expression was determined by real time RT-PCR, western blots, and MTT assays. The results found were statistically significant and pave the way to future experiments.