Limits...
The Cell Surface Estrogen Receptor, G Protein- Coupled Receptor 30 (GPR30), is Markedly Down Regulated During Breast Tumorigenesis.

Poola I, Abraham J, Liu A, Marshalleck JJ, Dewitty RL - Breast Cancer (Auckl) (2008)

Bottom Line: GPR30 is a cell surface estrogen receptor that has been shown to mediate a number of non-genomic rapid effects of estrogen and appear to balance the signaling of estrogen and growth factors.We compared its expression at mRNA levels by RT quantitative real-time PCR relative to GAPDH in ERα"-positive (n = 54) and ERα"-negative (n = 45) breast cancer tissues to their matched normal tissues.We report here, for the first time, that GPR30 mRNA levels were significantly down-regulated in cancer tissues in comparison with their matched normal tissues (p < 0.0001 by two sided paired t-test).

View Article: PubMed Central - PubMed

Affiliation: Department of Surgery and Breast Center and.

ABSTRACT

Background: GPR30 is a cell surface estrogen receptor that has been shown to mediate a number of non-genomic rapid effects of estrogen and appear to balance the signaling of estrogen and growth factors. In addition, progestins appear to use GPR30 for their actions. Therefore, GPR30 could play a critical role in hormonal regulation of breast epithelial cell integrity. Deregulation of the events mediated by GPR30 could contribute to tumorigenesis.

Methods: To understand the role of GPR30 in the deregulation of estrogen signaling processes during breast carcinogenesis, we have undertaken this study to investigate its expression at mRNA levels in tumor tissues and their matched normal tissues. We compared its expression at mRNA levels by RT quantitative real-time PCR relative to GAPDH in ERα"-positive (n = 54) and ERα"-negative (n = 45) breast cancer tissues to their matched normal tissues.

Results: We report here, for the first time, that GPR30 mRNA levels were significantly down-regulated in cancer tissues in comparison with their matched normal tissues (p < 0.0001 by two sided paired t-test). The GPR30 expression levels were significantly lower in tumor tissues from patients (n = 29) who had lymph node metastasis in comparison with tumors from patients (n = 53) who were negative for lymph node metastasis (two sample t-test, p < 0.02), but no association was found with ERα, PR and other tumor characteristics.

Conclusions: Down-regulation of GPR30 could contribute to breast tumorigenesis and lymph node metastasis.

No MeSH data available.


Related in: MedlinePlus

Tracings of amplification plots by RT Q real-time PCR showing expression of GPR30 in normal—tumor pairs. The RT Q real-time PCR for GPR30 was conducted as described in Materials and Methods. The mRNA expression levels were decreased significantly in tumor tissues (T) in comparison with their matched normal tissues (N). Examples of amplification plots for two matched normal-tumor pairs in ERα-positive and ERα-negative tumor groups are shown.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
getmorefigures.php?uid=PMC3091398&req=5

f2-bcbcr-2008-065: Tracings of amplification plots by RT Q real-time PCR showing expression of GPR30 in normal—tumor pairs. The RT Q real-time PCR for GPR30 was conducted as described in Materials and Methods. The mRNA expression levels were decreased significantly in tumor tissues (T) in comparison with their matched normal tissues (N). Examples of amplification plots for two matched normal-tumor pairs in ERα-positive and ERα-negative tumor groups are shown.

Mentions: We next quantified the GPR30 mRNA levels relative to the GAPDH levels in normal tissues and their matched tumor tissues using RT quantitative real-time PCR and comparative delta Ct method (14). By using these procedures we found that among the ERα- positive tissues, the mean GPR30 mRNA expression levels relative to GAPDH levels were 0.0058 (SD = 0.0075) in normal tissues and 0.0026 (SD = 0.0038) in cancer tissues. We next compared the relative expression levels between cancer tissues and their matched normal tissues using two- sided paired t-test. By applying this test, we found that GPR30 expression levels in cancer tissues was significantly lower than that in the normal tissues in a majority of cases (P = 0.0024; two-sided paired t-test). Among the ERα-negative samples, the relative mean GPR30 expression was 0.0067 (SD = 0.0081) in normal tissues and 0.0025 (SD = 0.0050) in cancer tissues. We observed a large standard deviation presumably because of very high variation in the individual tissues. The expression levels of GPR30 were also found to be significantly different between normal and ERα-negative cancer tissues (P < 0.0007; two-sided paired t-test). A statistically significant difference between normal and cancer tissues remains when all ERα-positive and ERα-negative tissues were combined (P < 0.0001; two-sided paired t-test). However, no significant difference was found in either normal or cancer tissue samples when we compared GPR30 mRNA levels between ERα-positive and ERα-negative tissues. (P = 0.5570 for normal samples, and P = 0.8980 for cancer samples by two-sided t-test). Quantitative data from 99 normal-tumor pairs are presented in Table 1. The mean expression values in each stage group in both ERα-positive and ERα-negative groups are shown in Table 2. Tracings of the amplification plots by Q real-time PCR for matched normal-tumor pairs two each from ERα-positive and ERα-negative groups are shown in Figure 2. The bar graphs showing the mean expression levels in tumors and normal tissues by Q real-time PCR are presented in Figure 3.


The Cell Surface Estrogen Receptor, G Protein- Coupled Receptor 30 (GPR30), is Markedly Down Regulated During Breast Tumorigenesis.

Poola I, Abraham J, Liu A, Marshalleck JJ, Dewitty RL - Breast Cancer (Auckl) (2008)

Tracings of amplification plots by RT Q real-time PCR showing expression of GPR30 in normal—tumor pairs. The RT Q real-time PCR for GPR30 was conducted as described in Materials and Methods. The mRNA expression levels were decreased significantly in tumor tissues (T) in comparison with their matched normal tissues (N). Examples of amplification plots for two matched normal-tumor pairs in ERα-positive and ERα-negative tumor groups are shown.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC3091398&req=5

f2-bcbcr-2008-065: Tracings of amplification plots by RT Q real-time PCR showing expression of GPR30 in normal—tumor pairs. The RT Q real-time PCR for GPR30 was conducted as described in Materials and Methods. The mRNA expression levels were decreased significantly in tumor tissues (T) in comparison with their matched normal tissues (N). Examples of amplification plots for two matched normal-tumor pairs in ERα-positive and ERα-negative tumor groups are shown.
Mentions: We next quantified the GPR30 mRNA levels relative to the GAPDH levels in normal tissues and their matched tumor tissues using RT quantitative real-time PCR and comparative delta Ct method (14). By using these procedures we found that among the ERα- positive tissues, the mean GPR30 mRNA expression levels relative to GAPDH levels were 0.0058 (SD = 0.0075) in normal tissues and 0.0026 (SD = 0.0038) in cancer tissues. We next compared the relative expression levels between cancer tissues and their matched normal tissues using two- sided paired t-test. By applying this test, we found that GPR30 expression levels in cancer tissues was significantly lower than that in the normal tissues in a majority of cases (P = 0.0024; two-sided paired t-test). Among the ERα-negative samples, the relative mean GPR30 expression was 0.0067 (SD = 0.0081) in normal tissues and 0.0025 (SD = 0.0050) in cancer tissues. We observed a large standard deviation presumably because of very high variation in the individual tissues. The expression levels of GPR30 were also found to be significantly different between normal and ERα-negative cancer tissues (P < 0.0007; two-sided paired t-test). A statistically significant difference between normal and cancer tissues remains when all ERα-positive and ERα-negative tissues were combined (P < 0.0001; two-sided paired t-test). However, no significant difference was found in either normal or cancer tissue samples when we compared GPR30 mRNA levels between ERα-positive and ERα-negative tissues. (P = 0.5570 for normal samples, and P = 0.8980 for cancer samples by two-sided t-test). Quantitative data from 99 normal-tumor pairs are presented in Table 1. The mean expression values in each stage group in both ERα-positive and ERα-negative groups are shown in Table 2. Tracings of the amplification plots by Q real-time PCR for matched normal-tumor pairs two each from ERα-positive and ERα-negative groups are shown in Figure 2. The bar graphs showing the mean expression levels in tumors and normal tissues by Q real-time PCR are presented in Figure 3.

Bottom Line: GPR30 is a cell surface estrogen receptor that has been shown to mediate a number of non-genomic rapid effects of estrogen and appear to balance the signaling of estrogen and growth factors.We compared its expression at mRNA levels by RT quantitative real-time PCR relative to GAPDH in ERα"-positive (n = 54) and ERα"-negative (n = 45) breast cancer tissues to their matched normal tissues.We report here, for the first time, that GPR30 mRNA levels were significantly down-regulated in cancer tissues in comparison with their matched normal tissues (p < 0.0001 by two sided paired t-test).

View Article: PubMed Central - PubMed

Affiliation: Department of Surgery and Breast Center and.

ABSTRACT

Background: GPR30 is a cell surface estrogen receptor that has been shown to mediate a number of non-genomic rapid effects of estrogen and appear to balance the signaling of estrogen and growth factors. In addition, progestins appear to use GPR30 for their actions. Therefore, GPR30 could play a critical role in hormonal regulation of breast epithelial cell integrity. Deregulation of the events mediated by GPR30 could contribute to tumorigenesis.

Methods: To understand the role of GPR30 in the deregulation of estrogen signaling processes during breast carcinogenesis, we have undertaken this study to investigate its expression at mRNA levels in tumor tissues and their matched normal tissues. We compared its expression at mRNA levels by RT quantitative real-time PCR relative to GAPDH in ERα"-positive (n = 54) and ERα"-negative (n = 45) breast cancer tissues to their matched normal tissues.

Results: We report here, for the first time, that GPR30 mRNA levels were significantly down-regulated in cancer tissues in comparison with their matched normal tissues (p < 0.0001 by two sided paired t-test). The GPR30 expression levels were significantly lower in tumor tissues from patients (n = 29) who had lymph node metastasis in comparison with tumors from patients (n = 53) who were negative for lymph node metastasis (two sample t-test, p < 0.02), but no association was found with ERα, PR and other tumor characteristics.

Conclusions: Down-regulation of GPR30 could contribute to breast tumorigenesis and lymph node metastasis.

No MeSH data available.


Related in: MedlinePlus