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Tumor-suppressor activity of RRIG1 in breast cancer.

Zhang G, Brewster A, Guan B, Fan Z, Brown PH, Xu XC - BMC Cancer (2011)

Bottom Line: Reverse-transcription polymerase chain reaction and western blot assays were used to detect the changes in gene expression.The immunohistochemical data showed that RRIG1 expression was reduced in breast cancer tissues compared with normal and atypical hyperplastic breast tissues.Expression of RRIG1 also reduced phosphorylated Erk1/2 and Akt levels; c-Jun, MMP9, and Akt expressions; and RhoA activity.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Clinical Cancer Prevention, The University of Texas M D Anderson Cancer Center, Houston, Texas 77030, USA.

ABSTRACT

Background: Retinoid receptor-induced gene-1 (RRIG1) is a novel gene that has been lost in several types of human cancers. The aim of this study was to determine whether RRIG1 plays a role in breast cancer, such as in the suppression of breast cancer cell growth and invasion.

Methods: Immunohistochemistry was used to detect RRIG1 expression in breast tissue specimens. Gene transfection was used to restore or knock down RRIG1 expression in breast cancer cell lines for analysis of cell viability, colony formation, and migration/invasion potential. Reverse-transcription polymerase chain reaction and western blot assays were used to detect the changes in gene expression. The RhoA activation assay was used to assess RRIG1-induced inhibition of RhoA activity.

Results: The immunohistochemical data showed that RRIG1 expression was reduced in breast cancer tissues compared with normal and atypical hyperplastic breast tissues. RRIG1 expression was inversely correlated with lymph node metastasis of breast cancer but was not associated with the status of hormone receptors, such as estrogen receptor, progesterone receptor, or HER2. Furthermore, restoration of RRIG1 expression inhibited proliferation, colony formation, migration, and invasion of breast cancer cells. Expression of RRIG1 also reduced phosphorylated Erk1/2 and Akt levels; c-Jun, MMP9, and Akt expressions; and RhoA activity. In contrast, knockdown of RRIG1 expression promoted breast cancer cell proliferation, colony formation, migration, and invasion potential.

Conclusion: The data from the current study indicated that RRIG1 expression was reduced or lost in breast cancer and that restoration of RRIG1 expression suppressed breast cancer cell growth and invasion capacity. Future studies will determine the underlying molecular mechanisms and define RRIG1 as a tumor-suppressor gene in breast cancer.

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Immunohistochemical analysis of RRIG1 expression. Breast tissue sections were immunostained with the rabbit polyclonal anti-RRIG1 antibody. DCIS, ductal carcinoma in situ.
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Figure 1: Immunohistochemical analysis of RRIG1 expression. Breast tissue sections were immunostained with the rabbit polyclonal anti-RRIG1 antibody. DCIS, ductal carcinoma in situ.

Mentions: To determine whether this antibody could be used for immunohistochemistry, we compared the data between immunohistochemistry and in situ hybridization for expression of RRIG1 mRNA and protein in the matched cells and tissues (Additional Figure S1cd). These data suggest that this antibody is suitable for immunohistochemistry. Next, we used immunohistochemical analysis to determine the RRIG1 expression in breast tissue specimens and found that RRIG1 was expressed in 14 of 15 normal mammary glands, 8 of 9 cases of atypical hyperplasia of the mammary gland, 6 of 10 ductal carcinoma in situ tissues, and 50 of 77 invasive breast cancer tissues (P = 0.023 between normal and invasive cancer by Fisher exact test) (Figure 1).


Tumor-suppressor activity of RRIG1 in breast cancer.

Zhang G, Brewster A, Guan B, Fan Z, Brown PH, Xu XC - BMC Cancer (2011)

Immunohistochemical analysis of RRIG1 expression. Breast tissue sections were immunostained with the rabbit polyclonal anti-RRIG1 antibody. DCIS, ductal carcinoma in situ.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3037341&req=5

Figure 1: Immunohistochemical analysis of RRIG1 expression. Breast tissue sections were immunostained with the rabbit polyclonal anti-RRIG1 antibody. DCIS, ductal carcinoma in situ.
Mentions: To determine whether this antibody could be used for immunohistochemistry, we compared the data between immunohistochemistry and in situ hybridization for expression of RRIG1 mRNA and protein in the matched cells and tissues (Additional Figure S1cd). These data suggest that this antibody is suitable for immunohistochemistry. Next, we used immunohistochemical analysis to determine the RRIG1 expression in breast tissue specimens and found that RRIG1 was expressed in 14 of 15 normal mammary glands, 8 of 9 cases of atypical hyperplasia of the mammary gland, 6 of 10 ductal carcinoma in situ tissues, and 50 of 77 invasive breast cancer tissues (P = 0.023 between normal and invasive cancer by Fisher exact test) (Figure 1).

Bottom Line: Reverse-transcription polymerase chain reaction and western blot assays were used to detect the changes in gene expression.The immunohistochemical data showed that RRIG1 expression was reduced in breast cancer tissues compared with normal and atypical hyperplastic breast tissues.Expression of RRIG1 also reduced phosphorylated Erk1/2 and Akt levels; c-Jun, MMP9, and Akt expressions; and RhoA activity.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Clinical Cancer Prevention, The University of Texas M D Anderson Cancer Center, Houston, Texas 77030, USA.

ABSTRACT

Background: Retinoid receptor-induced gene-1 (RRIG1) is a novel gene that has been lost in several types of human cancers. The aim of this study was to determine whether RRIG1 plays a role in breast cancer, such as in the suppression of breast cancer cell growth and invasion.

Methods: Immunohistochemistry was used to detect RRIG1 expression in breast tissue specimens. Gene transfection was used to restore or knock down RRIG1 expression in breast cancer cell lines for analysis of cell viability, colony formation, and migration/invasion potential. Reverse-transcription polymerase chain reaction and western blot assays were used to detect the changes in gene expression. The RhoA activation assay was used to assess RRIG1-induced inhibition of RhoA activity.

Results: The immunohistochemical data showed that RRIG1 expression was reduced in breast cancer tissues compared with normal and atypical hyperplastic breast tissues. RRIG1 expression was inversely correlated with lymph node metastasis of breast cancer but was not associated with the status of hormone receptors, such as estrogen receptor, progesterone receptor, or HER2. Furthermore, restoration of RRIG1 expression inhibited proliferation, colony formation, migration, and invasion of breast cancer cells. Expression of RRIG1 also reduced phosphorylated Erk1/2 and Akt levels; c-Jun, MMP9, and Akt expressions; and RhoA activity. In contrast, knockdown of RRIG1 expression promoted breast cancer cell proliferation, colony formation, migration, and invasion potential.

Conclusion: The data from the current study indicated that RRIG1 expression was reduced or lost in breast cancer and that restoration of RRIG1 expression suppressed breast cancer cell growth and invasion capacity. Future studies will determine the underlying molecular mechanisms and define RRIG1 as a tumor-suppressor gene in breast cancer.

Show MeSH
Related in: MedlinePlus