Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

NUCKS1 promotes breast cancer cell proliferation and metastasis via PI3K/ AKT pathway

Song Li¹, Daoliang Wang²

¹Department of Head and Neck Oncology, Edong Healthcare Huangshi Central Hospital, Huangshi, Hubei Province 435000, China; ²Department of Breast Surgery, Jingzhou First Peopleâ€™s Hospital, Jingzhou, Hubei Province 434000, China.

For correspondence:- Daoliang Wang Email: dlwang8972@163.com Tel:+8618163138972

Accepted: 26 September 2022 Published: 28 October 2022

Citation: Li S, Wang D. NUCKS1 promotes breast cancer cell proliferation and metastasis via PI3K/ AKT pathway. Trop J Pharm Res 2022; 21(10):2099-2105 doi: 10.4314/tjpr.v21i10.9

© 2022 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the role of nuclear casein kinase and cyclin-dependent kinase substrate 1 (NUCKS1) in breast cancer.

Methods: Breast cancer cells were maintained in RPMI-1640 medium containing 10 % fetal bovine serum in a incubator at 37 °C. Cell proliferation was determined by CCK8 and colony formation assays. Flow cytometry and Transwell assays were used to determine cell cycle and metastasis, respectively.

Results: expression of NUCKS1 was significantly elevated in breast cancer (p < 0.01). Overexpression of NUCKS1 significantly increased cell viability (p < 0.01), and promoted proliferation of breast cancer cells. Knockdown of NUCKS1 inhibited cell proliferation, and induced cell cycle arrest at G1 phase. However, overexpression of NUCKS1 promoted cell cycle progression via down-regulation of p21 and up-regulation of cyclin D1 and CDK1. Cell migration and invasion were induced by overexpression of NUCKS1, and suppressed by silencing of NUCKS1. Overexpression of NUCKS1 enhanced p-AKT and p-PI3K expression, while knockdown of NUCKS1 reduced the expression of p-AKT and p-PI3K in breast cancer cells.

Conclusion: NUCKS1 promotes breast cancer cell proliferation and metastasis via activation of PI3K/AKT signaling. The silencing of NUCKS1 can be used as a strategy to develop therapies for the management of breast cancer.

Keywords: NUCKS1, Breast cancer, Proliferation, Cycle, Migration, Invasion