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Cellular apoptosis susceptibility protein (CAS) suppresses the proliferation of breast cancer cells by upregulated cyp24a1

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Abstract

Breast cancer is the most common cancer in women. Although several studies demonstrated cellular apoptosis susceptibility protein (CAS) involved in the development of breast cancer, the underlying mechanisms of CAS regulating cell processes in the breast cancer remain elusive. In the present study, we explored the possible mechanism of CAS in contributing to the cell proliferation in the breast cancer cell line MCF-7. Knockdown of CAS led to the reduction of cell viability and proliferation. Furthermore, cell cycle was arrested in G0/G1 phase after knocking down CAS with the decrease of cyclinD1. In addition, RNA-seq analysis for the CAS knockdown cells demonstrated that total eleven genes were significantly altered (Fold changes > 2). Of note, the expression of cyp24a1 was dramatically increased in the shCAS cells compared to that of shNC cells as well as confirmed by quantitative real-time polymerase chain reaction (qPCR). These observations clarified the previous conflicting results on the cell fates of the breast cells regulated by CAS and provide new insight into the role of CAS in the development of breast cancer.

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Funding

This work was supported in part by grants from the National Key Research and Development Program of China (No. 2018YFC1003602 to HC); National Natural Science Foundation of China (81671432 and 81871202 to HC) and the startup R&D funding of Nantong University (03083011 and 03083028 to HC).

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HC conceived and designed the experiments. MY and XDW performed the experiments and analyzed the data. AZZ and FHL gave intelligent advice, JWS revised the manuscript, and MY, RGH and HC wrote the paper.

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Correspondence to Fanghong Li or Hao Chen.

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Hao Chen is the primary corresponding author.

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Ye, M., Han, R., Shi, J. et al. Cellular apoptosis susceptibility protein (CAS) suppresses the proliferation of breast cancer cells by upregulated cyp24a1. Med Oncol 37, 43 (2020). https://doi.org/10.1007/s12032-020-01366-w

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