Objective:
Sterol Regulatory Element Binding Transcription Factor 1 (SREBF1) encodes a core protein that has a crucial function in the metabolism of cholesterol and lipids. This transcription factor is a member of the family of transcription factors and highly expressed in a variety of cancer types. As of now, there are few reports on the relationship between the expression of SREBF1 and colon adenocarcinoma (COAD). Hence, this study utilizes databases and a range of experiments to explore the relationship between the expression of SREBF1 and tumor immune infiltration, as well as the occurrence and development of tumors.
Material and Methods:
The expression of SREBF1 in pan-cancers was retrieved through databases such as TIMER, Gene Expression Profiling Interactive Analysis (GEPIA), and UALCAN. The expression of SREBF1 in HCT-116 and SW480 cells was detected using western blot. Furthermore, we also found that knockdown SREBF1 can inhibit the proliferation and migration of COAD cells. The correlation between SREBF1 and autophagy in COAD cells was detected using acridine orange (AO) staining, western blot, and immunofluorescence (IF).
Results:
The databases of TIMER, GEPIA and UALCAN revealed that SREBF1 is overexpressed in pan-cancer tissues, and closely associated with the prognosis of the patients with cancer. Further immunohistochemical staining showed that SREBF1 was overexpressed in COAD, and closely related to the clinical stage and lymph node metastasis. Western blot revealed that SREBF1 was significantly expressed in both HCT-116 and SW480 COAD cells; knockdown of SREBF1 could inhibit the proliferation, DNA replication, and migration of COAD cells. The AO staining, western blot, and IF experiments also showed that silencing SREBF1 could promote the autophagy of COAD cell. Meanwhile, the TIMER database indicates a significant positive correlation between the presence of immune cells in COAD and variations in copy number alteration of SREBF1.
Conclusion:
SREBF1 might serve as a potential prognostic marker for COAD and be associated with immune cell infiltration.