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Overexpression of MTA3 Correlates with Tumor Progression in Non-Small Cell Lung Cancer.

Li H, Sun L, Xu Y, Li Z, Luo W, Tang Z, Qiu X, Wang E - PLoS ONE (2013)

Bottom Line: In addition, the depletion of MTA3 expression with small interfering RNAs inhibited cell growth and colony formation in the A549 and H157 lung cancer cell lines.Moreover, MTA3 depletion induced cell cycle arrest at the G1/S boundary.Western blotting analysis revealed that the knockdown of MTA3 decreased the protein levels of cyclin A, cyclin D1 and p-Rb.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, First Affiliated Hospital and College of Basic Medical Sciences, China Medical University, Shenyang, Liaoning, China.

ABSTRACT
The objective of the current study was to investigate the expression pattern and clinicopathological significance of MTA3 in patients with non-small cell lung cancer (NSCLC). The expression profile of MTA3 in NSCLC tissues and adjacent noncancerous lung tissues was detected by immunohistochemistry. MTA3 was overexpressed in 62 of 108 (57.4%) human lung cancer samples and correlated with p-TNM stage (p<0.0001), nodal metastasis (p = 0.0009) and poor prognosis (p<0.05). In addition, the depletion of MTA3 expression with small interfering RNAs inhibited cell growth and colony formation in the A549 and H157 lung cancer cell lines. Moreover, MTA3 depletion induced cell cycle arrest at the G1/S boundary. Western blotting analysis revealed that the knockdown of MTA3 decreased the protein levels of cyclin A, cyclin D1 and p-Rb. These results indicate that MTA3 plays an important role in NSCLC progression.

No MeSH data available.


Related in: MedlinePlus

MTA3 depletion impaired cancer cell proliferation.A. CCK-8 assay was performed after MTA3 siRNA treatment. A reduction of absorbance was observed (p<0.05 at day 5 for both A549 and H157). B. Assessment of clonogenic potentials of the MTA3-depleted cancer cells. Numbers of colonies were counted. The number of colonies formed by cells treated with MTA3 siRNA was far less than that of control cells (p<0.05). Columns, mean; bars, SD. *p<0.05.
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pone-0066679-g004: MTA3 depletion impaired cancer cell proliferation.A. CCK-8 assay was performed after MTA3 siRNA treatment. A reduction of absorbance was observed (p<0.05 at day 5 for both A549 and H157). B. Assessment of clonogenic potentials of the MTA3-depleted cancer cells. Numbers of colonies were counted. The number of colonies formed by cells treated with MTA3 siRNA was far less than that of control cells (p<0.05). Columns, mean; bars, SD. *p<0.05.

Mentions: The expression of MTA3 was analyzed through Western blotting and realtime PCR in a panel of lung cancer cell lines (Figure 3 A, B). We found that the level of MTA3 expression in H157 and A549 cells was higher than other cell lines.To explore the biological function of MTA3 in lung cancer cells, we employed siRNA to knockdown MTA3 expression in both H157 and A549 cell lines. Two MTA3 siRNAs (a and b), targeting different MTA3 sequences, were evaluated. The siRNAa was more effective at reducing MTA3 expression; thus we used it for further studies (Figure 3 C, D). To confirm the ability of siRNAa to downregulate MTA3 (and thus its transcriptional repression functions) we also examined the expression of the MTA3 downstream target genes Snail and Slug. As expected, treatment with MTA3 siRNAa upregulated the mRNA expression of Snail (Figure 3E). CCK-8 assay showed that MTA3 depletion reduced cell proliferaion in both cell lines. Colony formation analysis showed that the depletion of MTA3 in H157 and A549 cells led to a significant reduction in the number and size of foci (A549 control vs MTA3si: 275±7 vs 81±10; H157 control vs MTA3si: 476±10 vs 276±32), suggesting that MTA3 modulates the proliferation of lung cancer cells (Figure 4).


Overexpression of MTA3 Correlates with Tumor Progression in Non-Small Cell Lung Cancer.

Li H, Sun L, Xu Y, Li Z, Luo W, Tang Z, Qiu X, Wang E - PLoS ONE (2013)

MTA3 depletion impaired cancer cell proliferation.A. CCK-8 assay was performed after MTA3 siRNA treatment. A reduction of absorbance was observed (p<0.05 at day 5 for both A549 and H157). B. Assessment of clonogenic potentials of the MTA3-depleted cancer cells. Numbers of colonies were counted. The number of colonies formed by cells treated with MTA3 siRNA was far less than that of control cells (p<0.05). Columns, mean; bars, SD. *p<0.05.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3686714&req=5

pone-0066679-g004: MTA3 depletion impaired cancer cell proliferation.A. CCK-8 assay was performed after MTA3 siRNA treatment. A reduction of absorbance was observed (p<0.05 at day 5 for both A549 and H157). B. Assessment of clonogenic potentials of the MTA3-depleted cancer cells. Numbers of colonies were counted. The number of colonies formed by cells treated with MTA3 siRNA was far less than that of control cells (p<0.05). Columns, mean; bars, SD. *p<0.05.
Mentions: The expression of MTA3 was analyzed through Western blotting and realtime PCR in a panel of lung cancer cell lines (Figure 3 A, B). We found that the level of MTA3 expression in H157 and A549 cells was higher than other cell lines.To explore the biological function of MTA3 in lung cancer cells, we employed siRNA to knockdown MTA3 expression in both H157 and A549 cell lines. Two MTA3 siRNAs (a and b), targeting different MTA3 sequences, were evaluated. The siRNAa was more effective at reducing MTA3 expression; thus we used it for further studies (Figure 3 C, D). To confirm the ability of siRNAa to downregulate MTA3 (and thus its transcriptional repression functions) we also examined the expression of the MTA3 downstream target genes Snail and Slug. As expected, treatment with MTA3 siRNAa upregulated the mRNA expression of Snail (Figure 3E). CCK-8 assay showed that MTA3 depletion reduced cell proliferaion in both cell lines. Colony formation analysis showed that the depletion of MTA3 in H157 and A549 cells led to a significant reduction in the number and size of foci (A549 control vs MTA3si: 275±7 vs 81±10; H157 control vs MTA3si: 476±10 vs 276±32), suggesting that MTA3 modulates the proliferation of lung cancer cells (Figure 4).

Bottom Line: In addition, the depletion of MTA3 expression with small interfering RNAs inhibited cell growth and colony formation in the A549 and H157 lung cancer cell lines.Moreover, MTA3 depletion induced cell cycle arrest at the G1/S boundary.Western blotting analysis revealed that the knockdown of MTA3 decreased the protein levels of cyclin A, cyclin D1 and p-Rb.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, First Affiliated Hospital and College of Basic Medical Sciences, China Medical University, Shenyang, Liaoning, China.

ABSTRACT
The objective of the current study was to investigate the expression pattern and clinicopathological significance of MTA3 in patients with non-small cell lung cancer (NSCLC). The expression profile of MTA3 in NSCLC tissues and adjacent noncancerous lung tissues was detected by immunohistochemistry. MTA3 was overexpressed in 62 of 108 (57.4%) human lung cancer samples and correlated with p-TNM stage (p<0.0001), nodal metastasis (p = 0.0009) and poor prognosis (p<0.05). In addition, the depletion of MTA3 expression with small interfering RNAs inhibited cell growth and colony formation in the A549 and H157 lung cancer cell lines. Moreover, MTA3 depletion induced cell cycle arrest at the G1/S boundary. Western blotting analysis revealed that the knockdown of MTA3 decreased the protein levels of cyclin A, cyclin D1 and p-Rb. These results indicate that MTA3 plays an important role in NSCLC progression.

No MeSH data available.


Related in: MedlinePlus