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Published on: January 7, 2019
Tumor suppressor gene DLC1: Its modifications, interactive molecules, and potential prospects for clinical cancer
1Shandong Provincial Key Laboratory of Animal Resistant, School of Life Sciences, Shandong Normal University, Jinan, China.
Abstract:
Deleted in liver cancer 1 (DLC1) is a recognized tumor suppressor gene that negatively regulates Rho family proteins by hydrolyzing the active GTP-bound state to its inactive GDP-bound state. Active Rho proteins play a positive role in tumorigenesis. Numerous in vitro and in vivo experiments have shown that DLC1 is downregulated or inactivated in various solid tumors, which may be due to the following five reasons: genomic deletion, epigenetic modification and ubiquitin-dependent proteasomal degradation may cause DLC1 underexpression; phosphorylation at the post-translation level may cause DLC1 inactivation; and failure to localize at focal adhesions (FAs) may prevent DLC1 from exerting full activity. All of the causes could be attributed to molecular binding. Experimental evidence suggests that direct or indirect targeting of DLC1 is feasible for cancer treatment. Therefore, elucidating the interaction of DLC1 with its binding partners might provide novel targeted therapies for cancer. In this review, we summarized the binding partners of DLC1 at both the gene and protein levels and expounded a variety of anticancer drugs targeting DLC1 to provide information about DLC1 as a cancer diagnostic indicator or therapeutic target.
Insights
Deleted in liver cancer 1 (DLC1) is a tumor suppressor. This review explores DLC1
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- The tumor suppressor gene Deleted in liver cancer 1 (DLC1) negatively regulates Rho GTPases.
- DLC1 dysfunction is implicated in various solid tumors due to underexpression or inactivation.
- Mechanisms include genomic alterations, epigenetic changes, degradation, altered phosphorylation, and localization issues.
Purpose of the Study:
- To review the binding partners of DLC1 at the gene and protein levels.
- To explore anticancer drugs targeting DLC1.
- To highlight DLC1's potential as a diagnostic indicator and therapeutic target in cancer.
Main Methods:
- Literature review of studies on DLC1 binding partners.
- Analysis of existing and potential therapeutic strategies targeting DLC1.
- Synthesis of information on DLC1's role in tumorigenesis and its interaction networks.
Main Results:
- DLC1 interacts with various partners at both gene and protein levels.
- Dysregulation of these interactions contributes to DLC1's tumor-suppressive function loss.
- Several therapeutic strategies targeting DLC1 are being investigated.
Conclusions:
- Understanding DLC1 binding partners is crucial for developing targeted cancer therapies.
- DLC1 represents a promising target for novel cancer treatments and diagnostics.
- Further research into DLC1 interactions may unlock new therapeutic avenues.
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