Knockdown of CSNK2β suppresses MDA-MB231 cell growth, induces apoptosis, inhibits migration and invasion

Authors

  • Shibendra Kumar Lal Karna Faculty of Life Science and Biotechnology, South Asian University, Akbar Bhawan, Chanakyapuri, New Delhi-110021, India
  • Bilal Ahmad Lone Faculty of Life Science and Biotechnology, South Asian University, Akbar Bhawan, Chanakyapuri, New Delhi-110021, India
  • Faiz Ahmad Faculty of Life Science and Biotechnology, South Asian University, Akbar Bhawan, Chanakyapuri, New Delhi-110021, India
  • Nerina Shahi Faculty of Life Science and Biotechnology, South Asian University, Akbar Bhawan, Chanakyapuri, New Delhi-110021, India
  • Yuba Raj Pokharel Faculty of Life Science and Biotechnology, South Asian University, New Delhi-110021, India, Phone no- +91-11-24122512, Fax no-+91-1124122511, E-mail: yrp@sau.ac.in

DOI:

https://doi.org/10.17179/excli2020-2363

Keywords:

CSNK2β, Breast cancer, apoptosis, migration

Abstract

Breast cancer is the most common cancer among women worldwide. Among different types of breast cancer known, treatment of triple-negative breast cancer is a major challenge because of its aggressiveness and poor prognosis; thus, identification of specific drivers is required for targeted therapies of breast cancer malignancy. Protein Casein Kinase (CSNK) is a serine/threonine kinase that exists as a tetrameric complex consisting of two catalytic (α and /or α') and two regulatory β subunits. CSNK2β can also function independently without catalytic subunits and exist as a distinct population in cells. This study aims to elucidate the role of Casein Kinase 2β (CSNK2β) gene in cell proliferation, cell cycle, migration and apoptosis of triple-negative breast cancer MDA-MB-231 cells. The silencing of CSNK2β in MDA-MB-231 cells resulted in decreased cell viability and colony formation. Cell cycle analysis showed a significant arrest of cells in G2M phase. Hoechst and CM-H2DCFDA staining showed nuclear condensation and augmented intracellular reactive oxygen species (ROS) production. Furthermore, silencing of CSNK2β in MDA-MB-231 cells modulated the apoptotic machinery- BAX, Bcl-xL, and caspase 3; autophagy machinery-Beclin-1 and LC3-1; and inhibited the vital markers (p-ERK, c-Myc, NF-κB, E2F1, PCNA, p38-α) associated with cell proliferation and DNA replication pathways. In addition, knockdown of CSNK2β also affected the migration potential of MDA-MB-231, as observed in the wound healing and transwell migration assays. Altogether, the study suggests that CSNK2β silencing may offer future therapeutic target in triple-negative breast cancer.

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Published

2020-09-07

How to Cite

Karna, S. K. L., Lone, B. A., Ahmad, F., Shahi, N., & Pokharel, Y. R. (2020). Knockdown of CSNK2β suppresses MDA-MB231 cell growth, induces apoptosis, inhibits migration and invasion. EXCLI Journal, 19, 1211–1226. https://doi.org/10.17179/excli2020-2363

Issue

Vol. 19 (2020)

Section

Original articles

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Copyright (c) 2020 Shibendra Kumar Lal Karna, Bilal Ahmad Lone, Faiz Ahmad, Nerina Shahi, Yuba Raj Pokharel

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