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DLC1 is a chromosome 8p tumor suppressor whose loss promotes hepatocellular carcinoma
Wen Xue1, Alexander Krasnitz, Robert Lucito
1Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA.
Abstract:
Deletions on chromosome 8p are common in human tumors, suggesting that one or more tumor suppressor genes reside in this region. Deleted in Liver Cancer 1 (DLC1) encodes a Rho-GTPase activating protein and is a candidate 8p tumor suppressor. We show that DLC1 knockdown cooperates with Myc to promote hepatocellular carcinoma in mice, and that reintroduction of wild-type DLC1 into hepatoma cells with low DLC1 levels suppresses tumor growth in situ. Cells with reduced DLC1 protein contain increased GTP-bound RhoA, and enforced expression a constitutively activated RhoA allele mimics DLC1 loss in promoting hepatocellular carcinogenesis. Conversely, down-regulation of RhoA selectively inhibits tumor growth of hepatoma cells with disabled DLC1. Our data validate DLC1 as a potent tumor suppressor gene and suggest that its loss creates a dependence on the RhoA pathway that may be targeted therapeutically.
Insights
Deleted in Liver Cancer 1 (DLC1) acts as a tumor suppressor gene. Its loss promotes liver cancer by activating the RhoA pathway, offering a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Chromosome 8p deletions are frequent in human cancers.
- Deleted in Liver Cancer 1 (DLC1) is a candidate tumor suppressor gene in this region.
- DLC1 encodes a Rho-GTPase activating protein, regulating cell processes.
Purpose of the Study:
- To investigate the role of DLC1 in hepatocellular carcinoma (HCC).
- To determine if DLC1 functions as a tumor suppressor in the liver.
- To explore the relationship between DLC1, Myc, and the RhoA pathway in liver cancer.
Main Methods:
- Utilized mouse models of hepatocellular carcinoma with DLC1 knockdown and Myc overexpression.
- Assessed tumor growth in vivo after reintroducing wild-type DLC1 into hepatoma cells.
- Measured GTP-bound RhoA levels in cells with varying DLC1 expression.
- Investigated the effect of RhoA pathway inhibition on tumor growth.
Main Results:
- DLC1 knockdown cooperated with Myc to promote HCC development in mice.
- Restoring DLC1 expression suppressed tumor growth in hepatoma cells.
- Reduced DLC1 levels led to increased GTP-bound RhoA.
- Inhibition of RhoA selectively reduced tumor growth in DLC1-deficient cells.
Conclusions:
- DLC1 is validated as a significant tumor suppressor gene in hepatocellular carcinoma.
- Loss of DLC1 function creates a dependency on the RhoA pathway for tumor growth.
- Targeting the RhoA pathway presents a potential therapeutic strategy for DLC1-deficient liver cancers.
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