Cell-type specificity of β-actin expression and its clinicopathological correlation in gastric adenocarcinoma

Shafqat A Khan; Monica Tyagi; Ajit K Sharma; Savio Barreto; Bhawna Sirohi; Mukta Ramadwar; Shailesh V Shrikhande; Sanjay Gupta

doi:10.3748/wjg.v20.i34.12202

Cell-type specificity of β-actin expression and its clinicopathological correlation in gastric adenocarcinoma

Shafqat A Khan, Monica Tyagi, Ajit K Sharma, Savio Barreto, Bhawna Sirohi, Mukta Ramadwar, Shailesh V Shrikhande, Sanjay Gupta

Research output: Contribution to journal › Article

10 Citations (Scopus)

Abstract

AIM: To investigate cell type specific distribution of β-actin expression in gastric adenocarcinoma and its correlation with clinicopathological parameters. METHODS: β-actin is a housekeeping gene, frequently used as loading control, but, differentially expresses in cancer. In gastric cancer, an overall increased expression of β-actin has been reported using tissue disruptive techniques. At present, no histological data is available to indicate its cell type-specific expression and distribution pattern. In the present study, we analyzed β-actin expression and distribution in paired normal and tumor tissue samples of gastric adenocarcinoma patients using immunohistochemistry (IHC), a tissue non-disruptive technique as well as tissue disruptive techniques like reverse transcriptase-polymerase chain reaction (RT-PCR) and western blotting. Correlation of β-actin level with clinicopathological parameters was done using univariate analysis. RESULTS: The results of this study showed significant overexpression, at both mRNA and protein level in tumor tissues as confirmed by RT-PCR (1.47 ± 0.13 vs 2.36 ± 0.16; P < 0.001) and western blotting (1.92 ± 0.26 vs 2.88 ± 0.32; P < 0.01). IHC revealed that β-actin expression is majorly distributed between epithelial and inflammatory cells of the tissues. Inflammatory cells showed a significantly higher expression compared to epithelial cells in normal (2.46 ± 0.13 vs 5.92 ± 0.23, P < 0.001), as well as, in tumor tissues (2.79 ± 0.24 vs 6.71 ± 0.14, P < 0.001). Further, comparison of immunostaining between normal and tumor tissues revealed that both epithelial and inflammatory cells overexpress β-actin in tumor tissues, however, significant difference was observed only in inflammatory cells (5.92 ± 0.23 vs 6.71 ± 0.14, P < 0.01). Moreover, combined expression in epithelial and inflammatory cells also showed significant increase (4.19 ± 0.15 vs 4.75 ± 0.14, P < 0.05) in tumor tissues. In addition, univariate analysis showed a positive correlation of β-actin level of inflammatory cells with tumor grade (P < 0.05) while epithelial cells exhibited negative correlation (P > 0.05). CONCLUSION: In gastric cancer, β-actin showed an overall higher expression predominantly contributed by inflammatory or tumor infiltrating immune cells of the tissue microenvironment and correlates with tumor grade.

Original language	English
Pages (from-to)	12202-12211
Number of pages	10
Journal	World Journal of Gastroenterology
Volume	20
Issue number	34
DOIs	https://doi.org/10.3748/wjg.v20.i34.12202
Publication status	Published - 14 Sep 2014
Externally published	Yes

Bibliographical note

Articles published by this open-access journal are distributed under the terms of the Creative Commons Attribution-Noncommercial (CC BY-NC 4.0) License, which permits use, distribution, and reproduction in any medium, provided the original work is properly cited, the use is non commercial and is otherwise in compliance with the license.

Keywords

beta-actin
protein expression
disease
Immunohistochemistry
Inflammatory cells
Epithelial cells
Tumor infiltrating immune cells
Adjacent mucosa
β-actin
Gastric cancer
Resection margin

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@article{d06cee0830e64cdbaceb18dcc459b689,

title = "Cell-type specificity of β-actin expression and its clinicopathological correlation in gastric adenocarcinoma",

abstract = "AIM: To investigate cell type specific distribution of β-actin expression in gastric adenocarcinoma and its correlation with clinicopathological parameters. METHODS: β-actin is a housekeeping gene, frequently used as loading control, but, differentially expresses in cancer. In gastric cancer, an overall increased expression of β-actin has been reported using tissue disruptive techniques. At present, no histological data is available to indicate its cell type-specific expression and distribution pattern. In the present study, we analyzed β-actin expression and distribution in paired normal and tumor tissue samples of gastric adenocarcinoma patients using immunohistochemistry (IHC), a tissue non-disruptive technique as well as tissue disruptive techniques like reverse transcriptase-polymerase chain reaction (RT-PCR) and western blotting. Correlation of β-actin level with clinicopathological parameters was done using univariate analysis. RESULTS: The results of this study showed significant overexpression, at both mRNA and protein level in tumor tissues as confirmed by RT-PCR (1.47 ± 0.13 vs 2.36 ± 0.16; P < 0.001) and western blotting (1.92 ± 0.26 vs 2.88 ± 0.32; P < 0.01). IHC revealed that β-actin expression is majorly distributed between epithelial and inflammatory cells of the tissues. Inflammatory cells showed a significantly higher expression compared to epithelial cells in normal (2.46 ± 0.13 vs 5.92 ± 0.23, P < 0.001), as well as, in tumor tissues (2.79 ± 0.24 vs 6.71 ± 0.14, P < 0.001). Further, comparison of immunostaining between normal and tumor tissues revealed that both epithelial and inflammatory cells overexpress β-actin in tumor tissues, however, significant difference was observed only in inflammatory cells (5.92 ± 0.23 vs 6.71 ± 0.14, P < 0.01). Moreover, combined expression in epithelial and inflammatory cells also showed significant increase (4.19 ± 0.15 vs 4.75 ± 0.14, P < 0.05) in tumor tissues. In addition, univariate analysis showed a positive correlation of β-actin level of inflammatory cells with tumor grade (P < 0.05) while epithelial cells exhibited negative correlation (P > 0.05). CONCLUSION: In gastric cancer, β-actin showed an overall higher expression predominantly contributed by inflammatory or tumor infiltrating immune cells of the tissue microenvironment and correlates with tumor grade.",

keywords = "beta-actin, protein expression, disease, Immunohistochemistry, Inflammatory cells, Epithelial cells, Tumor infiltrating immune cells, Adjacent mucosa, β-actin, Gastric cancer, Resection margin",

author = "Khan, {Shafqat A} and Monica Tyagi and Sharma, {Ajit K} and Savio Barreto and Bhawna Sirohi and Mukta Ramadwar and Shrikhande, {Shailesh V} and Sanjay Gupta",

note = "Articles published by this open-access journal are distributed under the terms of the Creative Commons Attribution-Noncommercial (CC BY-NC 4.0) License, which permits use, distribution, and reproduction in any medium, provided the original work is properly cited, the use is non commercial and is otherwise in compliance with the license.",

year = "2014",

month = sep,

day = "14",

doi = "10.3748/wjg.v20.i34.12202",

language = "English",

volume = "20",

pages = "12202--12211",

journal = "World journal of gastroenterology",

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Cell-type specificity of β-actin expression and its clinicopathological correlation in gastric adenocarcinoma. / Khan, Shafqat A; Tyagi, Monica; Sharma, Ajit K; Barreto, Savio; Sirohi, Bhawna; Ramadwar, Mukta; Shrikhande, Shailesh V; Gupta, Sanjay.

In: World Journal of Gastroenterology, Vol. 20, No. 34, 14.09.2014, p. 12202-12211.

Research output: Contribution to journal › Article

TY - JOUR

T1 - Cell-type specificity of β-actin expression and its clinicopathological correlation in gastric adenocarcinoma

AU - Khan, Shafqat A

AU - Tyagi, Monica

AU - Sharma, Ajit K

AU - Barreto, Savio

AU - Sirohi, Bhawna

AU - Ramadwar, Mukta

AU - Shrikhande, Shailesh V

AU - Gupta, Sanjay

N1 - Articles published by this open-access journal are distributed under the terms of the Creative Commons Attribution-Noncommercial (CC BY-NC 4.0) License, which permits use, distribution, and reproduction in any medium, provided the original work is properly cited, the use is non commercial and is otherwise in compliance with the license.

PY - 2014/9/14

Y1 - 2014/9/14

N2 - AIM: To investigate cell type specific distribution of β-actin expression in gastric adenocarcinoma and its correlation with clinicopathological parameters. METHODS: β-actin is a housekeeping gene, frequently used as loading control, but, differentially expresses in cancer. In gastric cancer, an overall increased expression of β-actin has been reported using tissue disruptive techniques. At present, no histological data is available to indicate its cell type-specific expression and distribution pattern. In the present study, we analyzed β-actin expression and distribution in paired normal and tumor tissue samples of gastric adenocarcinoma patients using immunohistochemistry (IHC), a tissue non-disruptive technique as well as tissue disruptive techniques like reverse transcriptase-polymerase chain reaction (RT-PCR) and western blotting. Correlation of β-actin level with clinicopathological parameters was done using univariate analysis. RESULTS: The results of this study showed significant overexpression, at both mRNA and protein level in tumor tissues as confirmed by RT-PCR (1.47 ± 0.13 vs 2.36 ± 0.16; P < 0.001) and western blotting (1.92 ± 0.26 vs 2.88 ± 0.32; P < 0.01). IHC revealed that β-actin expression is majorly distributed between epithelial and inflammatory cells of the tissues. Inflammatory cells showed a significantly higher expression compared to epithelial cells in normal (2.46 ± 0.13 vs 5.92 ± 0.23, P < 0.001), as well as, in tumor tissues (2.79 ± 0.24 vs 6.71 ± 0.14, P < 0.001). Further, comparison of immunostaining between normal and tumor tissues revealed that both epithelial and inflammatory cells overexpress β-actin in tumor tissues, however, significant difference was observed only in inflammatory cells (5.92 ± 0.23 vs 6.71 ± 0.14, P < 0.01). Moreover, combined expression in epithelial and inflammatory cells also showed significant increase (4.19 ± 0.15 vs 4.75 ± 0.14, P < 0.05) in tumor tissues. In addition, univariate analysis showed a positive correlation of β-actin level of inflammatory cells with tumor grade (P < 0.05) while epithelial cells exhibited negative correlation (P > 0.05). CONCLUSION: In gastric cancer, β-actin showed an overall higher expression predominantly contributed by inflammatory or tumor infiltrating immune cells of the tissue microenvironment and correlates with tumor grade.

AB - AIM: To investigate cell type specific distribution of β-actin expression in gastric adenocarcinoma and its correlation with clinicopathological parameters. METHODS: β-actin is a housekeeping gene, frequently used as loading control, but, differentially expresses in cancer. In gastric cancer, an overall increased expression of β-actin has been reported using tissue disruptive techniques. At present, no histological data is available to indicate its cell type-specific expression and distribution pattern. In the present study, we analyzed β-actin expression and distribution in paired normal and tumor tissue samples of gastric adenocarcinoma patients using immunohistochemistry (IHC), a tissue non-disruptive technique as well as tissue disruptive techniques like reverse transcriptase-polymerase chain reaction (RT-PCR) and western blotting. Correlation of β-actin level with clinicopathological parameters was done using univariate analysis. RESULTS: The results of this study showed significant overexpression, at both mRNA and protein level in tumor tissues as confirmed by RT-PCR (1.47 ± 0.13 vs 2.36 ± 0.16; P < 0.001) and western blotting (1.92 ± 0.26 vs 2.88 ± 0.32; P < 0.01). IHC revealed that β-actin expression is majorly distributed between epithelial and inflammatory cells of the tissues. Inflammatory cells showed a significantly higher expression compared to epithelial cells in normal (2.46 ± 0.13 vs 5.92 ± 0.23, P < 0.001), as well as, in tumor tissues (2.79 ± 0.24 vs 6.71 ± 0.14, P < 0.001). Further, comparison of immunostaining between normal and tumor tissues revealed that both epithelial and inflammatory cells overexpress β-actin in tumor tissues, however, significant difference was observed only in inflammatory cells (5.92 ± 0.23 vs 6.71 ± 0.14, P < 0.01). Moreover, combined expression in epithelial and inflammatory cells also showed significant increase (4.19 ± 0.15 vs 4.75 ± 0.14, P < 0.05) in tumor tissues. In addition, univariate analysis showed a positive correlation of β-actin level of inflammatory cells with tumor grade (P < 0.05) while epithelial cells exhibited negative correlation (P > 0.05). CONCLUSION: In gastric cancer, β-actin showed an overall higher expression predominantly contributed by inflammatory or tumor infiltrating immune cells of the tissue microenvironment and correlates with tumor grade.

KW - beta-actin

KW - protein expression

KW - disease

KW - Immunohistochemistry

KW - Inflammatory cells

KW - Epithelial cells

KW - Tumor infiltrating immune cells

KW - Adjacent mucosa

KW - β-actin

KW - Gastric cancer

KW - Resection margin

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U2 - 10.3748/wjg.v20.i34.12202

DO - 10.3748/wjg.v20.i34.12202

M3 - Article

VL - 20

SP - 12202

EP - 12211

JO - World journal of gastroenterology

JF - World journal of gastroenterology

SN - 1007-9327

IS - 34

ER -