SOX11 inhibits tumor proliferation and promotes cell adhesion mediated-drug resistance via a CD43 dependent manner in mantle cell lymphoma

Abstract

SOX11 is a critical biomarker for mantle cell lymphoma (MCL) diagnosis; however, its role remains unclear in MCL. Here, clinical-pathological analysis showed Ki67 index was negatively relevant to SOX11 expression only in CD43 positive cases. Coexpression of SOX11/CD43 indicated longer overall survival. In vitro, knockout/overexpression of SOX11 or CD43 promoted/inhibited cell proliferation respectively. CD43 overexpression reversed tumor proliferation induced by SOX11 knockdown. Furthermore, overexpressing/silencing the SOX11/CD43 gene affects phosphorylation of p38-MAPK while p38 inhibitor reversed proliferation induced by si-SOX11 or si-CD43, respectively. In CAM-DR model, both SOX11 and CD43 in MCL cells were elevated when co-cultured with M2-10B4 bone marrow fibroblasts or fibronectin. Knockdown/overexpression of SOX11 decreased/increased cell adhesion, respectively, and the effect induced by silencing SOX11 was reversed by overexpression of CD43. Collectively, SOX11 could inhibit tumor proliferation and promote CAM-DR in a CD43 dependent manner.

Keywords:

• Mantle cell lymphoma
• SOX11
• CD43
• proliferation
• cell adhesion mediated-drug resistance

Ethical approval

This study was approved by the Ethical Committee of Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology. All participants provided informed consent prior to this study.

Author contributions

Rumeng Yang performed the experiments, Zitian Huo and Yaqi Duan analysed the results and wrote the paper. Weilin Tong, Yiyun Zheng and Yinxia Su collected patient follow-up information and records. Liping Lou, Qian Zhang and Sanpeng Xu conducted IHC expreiments, Changqing Peng helped with IHC expreiments. Dong Kuang and Guoping Wang conceived and designed the study. All authors have reviewed the manuscript.

Disclosure statement

The authors declare that they have no conflicts of interest.

Data availability

We declare all data are available.

Additional information

Funding

This work was supported by the National Science Foundation of Hubei Priovince [2019CFB158] and National Natural Science Foundation of China [31271040, 81770263, 81974016].