219
Views
7
CrossRef citations to date
0
Altmetric
Original Articles: Research

The tumor suppressive role of inhibin βA in diffuse large B-cell lymphoma

, , , , , , & show all
Pages 1202-1212 | Received 17 Apr 2017, Accepted 21 Aug 2017, Published online: 07 Sep 2017
 

Abstract

INHBA (inhibin βA), a subunit of a ligand of the transforming growth factor-β superfamily, is known to play diverse roles in various solid tumors. However, its role in hematologic malignancies remains unexplored. Here, we investigated the function of INHBA in diffuse large B-cell lymphoma (DLBCL). Both mRNA and protein levels of INHBA were significantly downregulated in primary DLBCL tissues, irrespective of germinal center B-cell-like (GCB) or non-GCB subtype, compared to those in benign tonsils. The low level of INHBA in patients with de novo DLBCL was correlated with reduced overall and progression-free survival. Ectopic expression of INHBA in DLBCL cell lines (OCI-Ly01 and SUDHL-10) resulted in reduced cell proliferation, increased spontaneous apoptosis and arrested cell cycle in vitro and suppressed xenograft tumor growth in vivo. Moreover, INHBA enhanced the chemosensitivity of DLBCL cells. Thus, our results provide novel evidence that INHBA functions as a tumor suppressor in DLBCL.

Acknowledegments

The work was supported by the National Natural Science Foundation of China [81400098, 81172251, and 81301725], the Zhejiang Provincial Natural Science Foundation [LY17H160005], the K.C. Wong Magna Fund in Ningbo University and in part by the Intramural Research Program of the NIAID, NIH, Division of Intramural Research, National Institute of Allergy and Infectious Diseases.

Potential conflict of interest

Disclosure forms provided by the authors are available with the full text of this article online at https://doi.org/10.1080/10428194.2017.1372574.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.