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RASSF10 suppresses hepatocellular carcinoma growth by activating P53 signaling and methylation of RASSF10 is a docetaxel resistant marker.

Jin Y, Cao B, Zhang M, Zhan Q, Herman JG, Yu M, Guo M - Genes Cancer (2015)

Bottom Line: Our previous study found that RASSF10 suppresses colorectal cancer growth by activating P53 signaling.In conclusion, we demonstrated that RASSF10 is frequently methylated in human HCC and its methylation is a potential docetaxel resistant marker.Our data also indicate that RASSF10 suppresses human HCC growth by activating P53 signaling.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology & Hepatology, Chinese PLA General Hospital, Beijing, China ; Department of Interventional Radiology, Chinese PLA General Hospital, Beijing, China.

ABSTRACT
Hepatocellular carcinoma (HCC) is one of the most common malignances and the second leading cause of cancer related death worldwide. RASSF10 is located on chromosome 11p15.2, a region that shows frequent loss of heterozygosity (LOH) in several cancer types. Our previous study found that RASSF10 suppresses colorectal cancer growth by activating P53 signaling. To explore the epigenetic changes and the mechanism of RASSF10 in human HCC, 69 cases of primary HCC, twenty cases of normal liver tissue samples and 17 HCC cell lines were involved in this study. We found that RASSF10 was methylated in 82.6% (57/69) of human primary HCC and methylation of RASSF10 was significantly associated with tumor size (P < 0.05) and TNM stage (P < 0.05). The expression of RASSF10 was regulated by promoter region methylation. Restoration of RASSF10 expression suppressed cell proliferation, induced apoptosis and G2/M phase arrest, as well as sensitized cells to docetaxel and activated P53 signaling in HepG2 and QGY7703 cells. In conclusion, we demonstrated that RASSF10 is frequently methylated in human HCC and its methylation is a potential docetaxel resistant marker. Our data also indicate that RASSF10 suppresses human HCC growth by activating P53 signaling.

No MeSH data available.


Related in: MedlinePlus

The effect of RASSF10 on HCC cell proliferation(A) Growth curves represent the effects of unexpressed and re-expressed RASSF10 in HepG2 and QGY7703 cells analyzed by the MTT assay. Each experiment was repeated in triplicate. * P < 0.05. (B) Colony formation results show that the colony number was reduced by re-expression of RASSF10 in HepG2 and QGY7703 cells. Each experiment was repeated in triplicate. The average number of tumor clones is represented by the bar diagram. * P < 0.05.
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Figure 4: The effect of RASSF10 on HCC cell proliferation(A) Growth curves represent the effects of unexpressed and re-expressed RASSF10 in HepG2 and QGY7703 cells analyzed by the MTT assay. Each experiment was repeated in triplicate. * P < 0.05. (B) Colony formation results show that the colony number was reduced by re-expression of RASSF10 in HepG2 and QGY7703 cells. Each experiment was repeated in triplicate. The average number of tumor clones is represented by the bar diagram. * P < 0.05.

Mentions: To evaluate the effects of RASSF10 on HCC progression, cell viability and colony formation assays were employed. As shown in Figure 4A, cell viability was determined by the MTT assay. The OD values were 0.498 ± 0.017 vs. 0.432 ± 0.021 (P<0.05) in HepG2 cells and 0.519 ± 0.028 vs. 0.320 ± 0.014 (P<0.05) in QGY703 cells before and after restoration of RASSF10 expression. The cell viability was significantly reduced. The colony numbers were 121 ± 8 vs. 64 ± 4 in HepG2 cells and 362 ± 22 vs. 222 ± 34 in QGY7703 cells before and after re-expression of RASSF10. The colony number was significantly reduced after re-expression of RASSF10 in HCC cells (all P<0.05, Figure 4B). These results demonstrate that RASSF10 suppresses the proliferation of HCC cells.


RASSF10 suppresses hepatocellular carcinoma growth by activating P53 signaling and methylation of RASSF10 is a docetaxel resistant marker.

Jin Y, Cao B, Zhang M, Zhan Q, Herman JG, Yu M, Guo M - Genes Cancer (2015)

The effect of RASSF10 on HCC cell proliferation(A) Growth curves represent the effects of unexpressed and re-expressed RASSF10 in HepG2 and QGY7703 cells analyzed by the MTT assay. Each experiment was repeated in triplicate. * P < 0.05. (B) Colony formation results show that the colony number was reduced by re-expression of RASSF10 in HepG2 and QGY7703 cells. Each experiment was repeated in triplicate. The average number of tumor clones is represented by the bar diagram. * P < 0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4482244&req=5

Figure 4: The effect of RASSF10 on HCC cell proliferation(A) Growth curves represent the effects of unexpressed and re-expressed RASSF10 in HepG2 and QGY7703 cells analyzed by the MTT assay. Each experiment was repeated in triplicate. * P < 0.05. (B) Colony formation results show that the colony number was reduced by re-expression of RASSF10 in HepG2 and QGY7703 cells. Each experiment was repeated in triplicate. The average number of tumor clones is represented by the bar diagram. * P < 0.05.
Mentions: To evaluate the effects of RASSF10 on HCC progression, cell viability and colony formation assays were employed. As shown in Figure 4A, cell viability was determined by the MTT assay. The OD values were 0.498 ± 0.017 vs. 0.432 ± 0.021 (P<0.05) in HepG2 cells and 0.519 ± 0.028 vs. 0.320 ± 0.014 (P<0.05) in QGY703 cells before and after restoration of RASSF10 expression. The cell viability was significantly reduced. The colony numbers were 121 ± 8 vs. 64 ± 4 in HepG2 cells and 362 ± 22 vs. 222 ± 34 in QGY7703 cells before and after re-expression of RASSF10. The colony number was significantly reduced after re-expression of RASSF10 in HCC cells (all P<0.05, Figure 4B). These results demonstrate that RASSF10 suppresses the proliferation of HCC cells.

Bottom Line: Our previous study found that RASSF10 suppresses colorectal cancer growth by activating P53 signaling.In conclusion, we demonstrated that RASSF10 is frequently methylated in human HCC and its methylation is a potential docetaxel resistant marker.Our data also indicate that RASSF10 suppresses human HCC growth by activating P53 signaling.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology & Hepatology, Chinese PLA General Hospital, Beijing, China ; Department of Interventional Radiology, Chinese PLA General Hospital, Beijing, China.

ABSTRACT
Hepatocellular carcinoma (HCC) is one of the most common malignances and the second leading cause of cancer related death worldwide. RASSF10 is located on chromosome 11p15.2, a region that shows frequent loss of heterozygosity (LOH) in several cancer types. Our previous study found that RASSF10 suppresses colorectal cancer growth by activating P53 signaling. To explore the epigenetic changes and the mechanism of RASSF10 in human HCC, 69 cases of primary HCC, twenty cases of normal liver tissue samples and 17 HCC cell lines were involved in this study. We found that RASSF10 was methylated in 82.6% (57/69) of human primary HCC and methylation of RASSF10 was significantly associated with tumor size (P < 0.05) and TNM stage (P < 0.05). The expression of RASSF10 was regulated by promoter region methylation. Restoration of RASSF10 expression suppressed cell proliferation, induced apoptosis and G2/M phase arrest, as well as sensitized cells to docetaxel and activated P53 signaling in HepG2 and QGY7703 cells. In conclusion, we demonstrated that RASSF10 is frequently methylated in human HCC and its methylation is a potential docetaxel resistant marker. Our data also indicate that RASSF10 suppresses human HCC growth by activating P53 signaling.

No MeSH data available.


Related in: MedlinePlus