Jameka Grigsby¹*, Shavonda Jackson¹, Kenneth Duma², Ariane M Chitoh ³ and Clement G Yedjou ⁴

¹ Department of Biological Sciences, Alcorn State University, Lorman, MS, 39096, USA
² Department of Biology, Jackson State University, Jackson, MS, 39217, USA
³ RCMI Center for Health Disparities Research, Jackson State University, Jackson, MS, 39217, USA
⁴ Department of Biological Data Sciences, Florida Agricultural and Mechanical University, Tallahassee, FL 32307, USA

*Corresponding Author:Jameka Grigsby, Department of Biological Sciences, Alcorn State University, Lorman, MS, 39096, USA

Received: December 15, 2025; Published: January 31, 2026

Abstract

Pancreatic cancer is the most lethal of all cancers. Patients diagnosed with this disease die within six months 95% of the time. There is one currently known conventional chemotherapy for pancreatic cancer and it provides minimal benefits. This study’s recent strategic efforts have focused on identifying and validating improved molecular targets against pancreatic cancer. In this study, the potential role of Myosin Regulatory Light Chain (MRCL3) in pancreatic cancer was evaluated. MRCL3 is a regulatory protein implicated in cytokinesis, receptor capping, and cell locomotion. The effect of silencing MRCL3 in BxPC3 cells was examined to determine whether endogenous MRCL3 promoted growth in pancreatic cancer cells. This study demonstrated that MRCL3 significantly inhibited the proliferation of these cells compared with the controls. Cells undergoing apoptosis (Sub G1) were measured after transfecting BxPC3 cells with MRCL3 siRNA to determine whether MRCL3 is also required for protecting pancreatic cancer cells from cell death. Knockdown of MRCL3 resulted in 10% increase in cell death in BxPC3 cells compared to the controls. The expression of AP-1 protein factors, c-Fos and c-Jun, were examined in BxPC3 cells to investigate how MRCL3 regulated cell fate. This study has shown that MRCL3 knockdown in these cells increased the expression of c-Jun while blocking c-Fos expression. These results imply that the MRCL3 pathway is mediated through AP-1 transcriptional factors. Given the lack of promising pancreatic cancer drugs, this study sheds several insights on possible targets that can lead to the treatment of this disease.

Keywords: Myosin Regulatory Light Chain; Pancreatic Cancer; Proliferation (MTS) Assay; Western Blot; Phospho p53 Assay

References

1. Grant JW., et al. “Human Nonsarcomeric 20,000 Da Myosin Regulatory Light Chain cDNA”. Nucleic Acids Research19 (1990): 5892.
2. Watanabe, F., et al. “Purification, Some Properties and Possible Physiological Role of an Extracellular Cobalamin-Binding Protein from Euglena gracilis”. Journal of General Microbiology 134 (1988): 1385-1389.
3. Orr B., et al. “Identification of Stromally Expressed Molecules in the Prostate by Tag- Profiling of Cancer-Associated Fibroblasts, Normal Fibroblasts and Fetal Prostate”. Oncogene 31 (2012): 1130-1142.
4. Addou-Klouche L., et al. “Loss, Mutation and Deregulation of L3MBTL4 in Breast Cancers”. Molecular Cancer 9 (2010): 213.
5. Li P., et al. “Cytochrome c and dATP-Dependent Formation of Apaf-1/Caspase-9 Complex Initiates an Apoptotic Protease Cascade”. Cell4 (1997): 479-489.
6. Jin Z and W El-Deiry. “Overview of Cell Death Signaling Pathways”. Cancer Biology and Therapy2 (2005): 139-163.
7. Vogelstein B., et al. “Genetic Alterations during Colorectal-Tumor Development”. New England Journal of Medicine 319 (1988): 525-532.
8. Kastan M., et al. “DNA Damage Induces Phosphorylation of the Amino Terminus of p53”. Genes and Development 11 (1997): 3471-3481.
9. Whitmarsh A and R Davis. “Transcription Factor AP-1 Regulation by Mitogen- Activated Protein Kinase Signal Transduction Pathways”. Journal of Molecular Medicine (Berlin)10 (1996): 589-607.
10. Ozanne B., et al. “Transcription Factors Control Invasion: AP-1 the First among Equals”. Oncogene 26 (2007): 1-10.

Citation

Citation: Jameka Grigsby., et al. “Myosin Regulatory Light Chain Silencing: Function, Mechanisms, and Therapeutic Implications in Pancreatic Cancer". Acta Scientific Microbiology 9.2 (2026): 63-70.

Copyright

Copyright: © 2026 Jameka Grigsby., et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.