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In silico analysis of molecular mechanisms of legume lectin‐induced apoptosis in cancer cells
Author(s) -
Shi Z.,
An N.,
Zhao S.,
Li X.,
Bao J. K.,
Yue B. S.
Publication year - 2013
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/cpr.12009
Subject(s) - lectin , biology , receptor , in silico , cancer cell , microbiology and biotechnology , apoptosis , rna , biochemistry , cancer , gene , genetics
Objectives The legume lectin family, one of the most extensively studied plant lectin families, has received increasing attention for the remarkable anti‐tumor activities of its members for binding specific cancer cell surface glycoconjugates. MicroRNAs, a class of small, non‐coding RNAs, control translation and stability of mRNA s at post‐transcriptional and translational levels. To date, accumulating evidence has revealed that micro RNA s are involved in progression of a number of human diseases, especially cancers. However, the molecular manners of micro RNA ‐modulated apoptosis in legume lectin‐treated cancer cells are still under investigation. Materials and methods We performed in silico analyses to study the interactions between three typical legume lectins (ConA, SFL and SAL ) and some specific sugar‐containing receptors (for example, EGFR , TNFR 1, HSP 70 and HSP 90). Additionally, we predicted some relevant micro RNA s which could significantly regulate these aforementioned targetreceptors and thus inhibiting down‐stream cancer‐related signaling pathways. Results The results showed that these three legume lectins could competitively bind sugar‐containing receptors such as EGFR , TNFR 1, HSP 70 and HSP 90 in two ways, via anti‐apoptotic or survival pathways. On the one hand, the legume lectins could induce cancer cell death through triggering receptor‐mediated signaling pathways, which resulted from indirect binding between legume lectins and mannoses resided in receptors. On the other hand, direct binding between legume lectins and receptors could lead to steric hindrance, which would disturb efficient interactions between them, and thus, the legume lectins would induce cancer cell death by triggering receptor‐mediated signaling pathways. In addition, we identified several relevant micro RNA s that regulated these targeted receptors, thereby ultimately causing cancer cell apoptosis. Conclusions These findings provide new perspectives for exploring micro RNA ‐modulated cell death in legume lectin‐treated cancer cells, which could be utilized in combination therapy for future cancer drug development.

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