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- Title
Stratifin (SFN) regulates lung cancer progression via nucleating the Vps34‐BECN1‐TRAF6 complex for autophagy induction.
- Authors
Kim, Ji Young; Kim, Mi‐Jeong; Lee, Ji Su; Son, Juhee; Kim, Duk‐Hwan; Lee, Joo Sang; Jeong, Soo‐Kyung; Chun, Eunyoung; Lee, Ki‐Young
- Abstract
Moreover, 34 cancer suppressors genes were down-regulated in tumour tissues of the seven primary LUAD patients (Figure 2I, Table S8), and 18 genes were functionally associated with lung cancer (Figure 2I, green box; Table S8, green letters). Lung cancer progression is regulated by various extrinsic factors derived from tumour microenvironment as well as intrinsic factors.1 Recent studies have shown that toll-like receptors (TLRs) are expressed in lung cancers, suggesting that TLRs may be implicated in lung cancer progression.2,3 Although several studies have shown that stratifin ( I SFN i , 14-3-3 sigma) facilitated lung cancer development and progression,4-6 the molecular and cellular mechanisms by which I SFN i is functionally involved in lung cancer progression, and the role of I SFN i in lung cancer progression in response to extrinsic stimulation, such as TLR agonist, are largely unknown. Stratifin (SFN) regulates lung cancer progression via nucleating the Vps34-BECN1-TRAF6 complex for autophagy induction Importantly, the ubiquitination of BECN1 was markedly enhanced in the presence of SFN as compared to the absence of SFN (Figure 3F, lane 4 and 5 vs. lane 3), indicating that SFN nucleates the molecular association of TRAF6-BECN1 and enhances the ubiquitination of BECN1 (Figure 3G).
- Subjects
LUNG cancer; CANCER invasiveness; SIGMA receptors; AUTOPHAGY; TUMOR suppressor genes; NON-small-cell lung carcinoma
- Publication
Clinical & Translational Medicine, 2022, Vol 12, Issue 6, p1
- ISSN
2001-1326
- Publication type
Article
- DOI
10.1002/ctm2.896