Incorporation of human β-defensin-1 into immunoliposomes to facilitate targeted autophagy therapy of colon carcinoma

Table 1 Summary of the study of Zhao et al[1]

Section	Summary
Background	Colorectal cancer has a low 5-year survival rate and a high mortality rate. The hBD-1 may function in the innate immune system, which recognises and destroys cancer cells. LncRNAs are involved in cell differentiation and growth
Methods	Cell proliferation was detected using the cell counting kit 8 method to determine the optimal drug concentration. The effect of hBD-1 on the SW620 cell proliferation was evaluated by a colony formation assay. Bioinformatics was used to screen LncRNAs for potential biological significance associated with the mTOR pathway. In addition, the expression of p-mTOR, beclin1 and LC3I/II in the SW620 cells was detected by western blot analysis
Results	The hBD-1 inhibited the SW620 cell proliferation, as shown by the reduced colony-forming ability of SW620 cells following the hBD-1 exposure. The hBD-1 decreased the expression of the p-mTOR (Ser2448) protein and increased the expression of the Beclin1 and LC3II/I proteins. In addition, a bioinformatics analysis identified seven lncRNAs associated with the mTOR pathway (two up-regulated and five down-regulated). Finally, lncRNA TCONS_00014506 was selected. Following the lncRNA TCONS_00014506 inhibition, exposure to hBD-1 inhibited p-mTOR (Ser2448) and promoted beclin1 and LC3II/I protein expression
Conclusion	In the SW620 colon cancer cells, hBD-1 increased the lncRNA TCONS_00014506 expression to suppress the mTOR pathway and promote autophagy

HBD-1: Human β-defensin-1; LC3: Light chain 3; LncRNA: Long non-coding RNA; MTOR: Mammalian target of rapamycin.