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High expression of prolactin receptor is associated with cell survival in cervical cancer cells.

Lopez-Pulido EI, Muñoz-Valle JF, Del Toro-Arreola S, Jave-Suárez LF, Bueno-Topete MR, Estrada-Chávez C, Pereira-Suárez AL - Cancer Cell Int. (2013)

Bottom Line: The aim of this study was to evaluate the expression of PRL/PRLR and the effect of PRL treatment on cell proliferation and apoptosis in cervical cancer cell lines.Treatment with PRL (200 ng/ml) increased cell proliferation in HeLa cells determined by the MTT assay at day 3 and after 1 day a protective effect against etoposide induced apoptosis in HeLa, SiHa and C-33A cervical cancer cell lines analyzed by the TUNEL assay.The use of an effective PRL antagonist may provide a better therapeutic intervention in cervical cancer.

View Article: PubMed Central - HTML - PubMed

Affiliation: Laboratorio de Inmunología, Departamento de Fisiología, Centro Universitario de, Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, México. analauraps@hotmail.com.

ABSTRACT

Background: The altered expression of prolactin (PRL) and its receptor (PRLR) has been implicated in breast and other types of cancer. There are few studies that have focused on the analysis of PRL/PRLR in cervical cancer where the development of neoplastic lesions is influenced by the variation of the hormonal status. The aim of this study was to evaluate the expression of PRL/PRLR and the effect of PRL treatment on cell proliferation and apoptosis in cervical cancer cell lines.

Results: High expression of multiple PRLR forms and PRLvariants of 60-80 kDa were observed in cervical cancer cell lines compared with non-tumorigenic keratinocytes evaluated by Western blot, immunofluorecence and real time PCR. Treatment with PRL (200 ng/ml) increased cell proliferation in HeLa cells determined by the MTT assay at day 3 and after 1 day a protective effect against etoposide induced apoptosis in HeLa, SiHa and C-33A cervical cancer cell lines analyzed by the TUNEL assay.

Conclusions: Our data suggests that PRL/PRLR signaling could act as an important survival factor for cervical cancer. The use of an effective PRL antagonist may provide a better therapeutic intervention in cervical cancer.

No MeSH data available.


Related in: MedlinePlus

PRLR expression in human cervical cancer cells. SiHa, C-33A, HeLa (Cervical cancer cells) and control cells MCF-7, T-47D (breast cancer), HaCaT (Inmortalized human keratinocytes) were cultured in DMEM or RPMI medium containing 10% FBS. A) PRLR protein was determined by western blot using a specific antibody against the PRLR, PRLR proteins were identified by their size. B) Demonstration of the arbitrary optical density measurements from Western immunoblots assessing PRLR levels. C) The cells grown on coverslips were fixed, and the localization of PRLR (green) was observed by inmunocitochemistry using a secondary antibody conjugated with Alexa fluor 488 and DAPI stain (blue) to visualize the presence of cells. Magnification 10 x. D) Relative expression of PRLR mRNA was measure by quantitative RT-PCR.
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Figure 1: PRLR expression in human cervical cancer cells. SiHa, C-33A, HeLa (Cervical cancer cells) and control cells MCF-7, T-47D (breast cancer), HaCaT (Inmortalized human keratinocytes) were cultured in DMEM or RPMI medium containing 10% FBS. A) PRLR protein was determined by western blot using a specific antibody against the PRLR, PRLR proteins were identified by their size. B) Demonstration of the arbitrary optical density measurements from Western immunoblots assessing PRLR levels. C) The cells grown on coverslips were fixed, and the localization of PRLR (green) was observed by inmunocitochemistry using a secondary antibody conjugated with Alexa fluor 488 and DAPI stain (blue) to visualize the presence of cells. Magnification 10 x. D) Relative expression of PRLR mRNA was measure by quantitative RT-PCR.

Mentions: PRLR expression was assessed in cervical cancer cell lines (HeLa, SiHa and C-33A) and human non-tumorigenic keratinocytes (HaCaT) by western blot, immunocitochemistry and real time-PCR. Breast cancer cell lines T-47D and MCF-7 served as the positive control. To detect PRLR expression we used an antibody raised against amino acids 323–622 of human PRLR that recognized multiple isoforms. In T-47D and MCF-7 we observed a high expression of different bands (110 kDa, 90 kDa, 80 kDa, 60 kDa and 50 kDa) that corresponded to PRLR isoforms. Differently than breast cancer cells, in cervical cancer cell lines HeLa, SiHa and C-33A we detected three of the PRLR forms (110 kDa, 60 kDa and 50 kDa). However, human non-tumorigenic keratinocytes (HaCaT) only expressed low levels of the 50 kDa PRLR band (Figure 1A). The optical density measurements from immunoblots demonstrated higher PRLR expression in cancer cell lines in comparison with the non-tumorigenic HaCaT cell line (Figure 1B).


High expression of prolactin receptor is associated with cell survival in cervical cancer cells.

Lopez-Pulido EI, Muñoz-Valle JF, Del Toro-Arreola S, Jave-Suárez LF, Bueno-Topete MR, Estrada-Chávez C, Pereira-Suárez AL - Cancer Cell Int. (2013)

PRLR expression in human cervical cancer cells. SiHa, C-33A, HeLa (Cervical cancer cells) and control cells MCF-7, T-47D (breast cancer), HaCaT (Inmortalized human keratinocytes) were cultured in DMEM or RPMI medium containing 10% FBS. A) PRLR protein was determined by western blot using a specific antibody against the PRLR, PRLR proteins were identified by their size. B) Demonstration of the arbitrary optical density measurements from Western immunoblots assessing PRLR levels. C) The cells grown on coverslips were fixed, and the localization of PRLR (green) was observed by inmunocitochemistry using a secondary antibody conjugated with Alexa fluor 488 and DAPI stain (blue) to visualize the presence of cells. Magnification 10 x. D) Relative expression of PRLR mRNA was measure by quantitative RT-PCR.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4016267&req=5

Figure 1: PRLR expression in human cervical cancer cells. SiHa, C-33A, HeLa (Cervical cancer cells) and control cells MCF-7, T-47D (breast cancer), HaCaT (Inmortalized human keratinocytes) were cultured in DMEM or RPMI medium containing 10% FBS. A) PRLR protein was determined by western blot using a specific antibody against the PRLR, PRLR proteins were identified by their size. B) Demonstration of the arbitrary optical density measurements from Western immunoblots assessing PRLR levels. C) The cells grown on coverslips were fixed, and the localization of PRLR (green) was observed by inmunocitochemistry using a secondary antibody conjugated with Alexa fluor 488 and DAPI stain (blue) to visualize the presence of cells. Magnification 10 x. D) Relative expression of PRLR mRNA was measure by quantitative RT-PCR.
Mentions: PRLR expression was assessed in cervical cancer cell lines (HeLa, SiHa and C-33A) and human non-tumorigenic keratinocytes (HaCaT) by western blot, immunocitochemistry and real time-PCR. Breast cancer cell lines T-47D and MCF-7 served as the positive control. To detect PRLR expression we used an antibody raised against amino acids 323–622 of human PRLR that recognized multiple isoforms. In T-47D and MCF-7 we observed a high expression of different bands (110 kDa, 90 kDa, 80 kDa, 60 kDa and 50 kDa) that corresponded to PRLR isoforms. Differently than breast cancer cells, in cervical cancer cell lines HeLa, SiHa and C-33A we detected three of the PRLR forms (110 kDa, 60 kDa and 50 kDa). However, human non-tumorigenic keratinocytes (HaCaT) only expressed low levels of the 50 kDa PRLR band (Figure 1A). The optical density measurements from immunoblots demonstrated higher PRLR expression in cancer cell lines in comparison with the non-tumorigenic HaCaT cell line (Figure 1B).

Bottom Line: The aim of this study was to evaluate the expression of PRL/PRLR and the effect of PRL treatment on cell proliferation and apoptosis in cervical cancer cell lines.Treatment with PRL (200 ng/ml) increased cell proliferation in HeLa cells determined by the MTT assay at day 3 and after 1 day a protective effect against etoposide induced apoptosis in HeLa, SiHa and C-33A cervical cancer cell lines analyzed by the TUNEL assay.The use of an effective PRL antagonist may provide a better therapeutic intervention in cervical cancer.

View Article: PubMed Central - HTML - PubMed

Affiliation: Laboratorio de Inmunología, Departamento de Fisiología, Centro Universitario de, Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, México. analauraps@hotmail.com.

ABSTRACT

Background: The altered expression of prolactin (PRL) and its receptor (PRLR) has been implicated in breast and other types of cancer. There are few studies that have focused on the analysis of PRL/PRLR in cervical cancer where the development of neoplastic lesions is influenced by the variation of the hormonal status. The aim of this study was to evaluate the expression of PRL/PRLR and the effect of PRL treatment on cell proliferation and apoptosis in cervical cancer cell lines.

Results: High expression of multiple PRLR forms and PRLvariants of 60-80 kDa were observed in cervical cancer cell lines compared with non-tumorigenic keratinocytes evaluated by Western blot, immunofluorecence and real time PCR. Treatment with PRL (200 ng/ml) increased cell proliferation in HeLa cells determined by the MTT assay at day 3 and after 1 day a protective effect against etoposide induced apoptosis in HeLa, SiHa and C-33A cervical cancer cell lines analyzed by the TUNEL assay.

Conclusions: Our data suggests that PRL/PRLR signaling could act as an important survival factor for cervical cancer. The use of an effective PRL antagonist may provide a better therapeutic intervention in cervical cancer.

No MeSH data available.


Related in: MedlinePlus