176
Views
13
CrossRef citations to date
0
Altmetric
Original Research

Transcriptional regulation of Mcl-1 plays an important role of cellular protective effector of vincristine-triggered autophagy in oral cancer cells

, , , , &
 

Abstract

Objective: The autophagy-associated release of HMGB1 (high-mobility group box 1) has been reported that protect cancer cells from numerous chemotherapeutics. However, the related molecular mechanism involved in the protection of oral cancer cells remains unclear.

Research design and methods: In this study, we determined that HMGB1 released by oral cancer cells protected the cells against apoptosis caused by vincristine by upregulating the transcription of Mcl-1.

Results: Extracellular HMGB1 seems to be required for the autophagy-mediated inhibition of apoptosis because the effect of autophagy protection was abolished by HMGB1 knockdown. Vincristine treatment increased the expression of Mcl-1 mRNA, but decreased the Mcl-1 protein expression. HMGB1 expression inhibited blocked the Mcl-1 transcription increase and reduced Mcl-1 expression, demonstrate that HMGB1 is required for the upregulation of Mcl-1 transcriptional, and thereby maintaining Mcl-1 protein expression levels is required for the survival of oral cancer cells by vincristine.

Conclusions: Collectively, this study suggested that the HMGB1-mediated Mcl-1 transcription upregulation is a key mechanism by which autophagy protects oral cancer cells against vincristine-induced apoptosis.

View correction statement:
Corrigendum

Declaration of interest

This study was supported by grants from National Science Council, Taiwan (MOST 103-2314-B-371-007-MY2). The authors of the manuscript do not have a direct financial relation with the commercial identity mentioned in this paper. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Notes

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.