Bioinformatic analysis of the clinicopathological and prognostic significance of oocyte-arresting BTG4 mRNA expression in gynecological cancers

BTG4 arrests the cell cycle and suppresses oocyte and embryonic development. We performed a bioinformatic analysis of BTG4 expression. BTG4 expression was downregulated in breast cancer compared with normal tissues (p < .05), but the opposite was observed in cervical, endometrial and ovarian canc...

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Published inJournal of obstetrics and gynaecology Vol. 43; no. 1; p. 2182672
Main Authors Zheng, Hua-chuan, Xue, Hang, Zhang, Cong-yu, Zhang, Rui
Format Journal Article
LanguageEnglish
Published England Taylor & Francis 01.12.2023
Taylor & Francis Ltd
Taylor & Francis Group
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ISSN0144-3615
1364-6893
1364-6893
DOI10.1080/01443615.2023.2182672

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Abstract BTG4 arrests the cell cycle and suppresses oocyte and embryonic development. We performed a bioinformatic analysis of BTG4 expression. BTG4 expression was downregulated in breast cancer compared with normal tissues (p < .05), but the opposite was observed in cervical, endometrial and ovarian cancers (p < .05). BTG4 methylation was negatively correlated with its mRNA expression in breast, cervical and endometrial cancers (p < .05). BTG4 mRNA expression was negatively correlated with T staging and distant metastasis of breast cancer; and with tumor invasion, clinical stage, low weight and BMI, low histological grade and no diabetes in endometrial cancer but positively with T stage and non-keratinizing squamous carcinoma in endometrial cancer. BTG4 expression was negatively correlated with the survival of ovarian cancer patients (p < .05), but positively for breast, cervical and endometrial cancers (p < .05). BTG4 expression is thus a potential marker reflecting the carcinogenesis, aggressiveness and prognosis in gynecological cancers. Impact Statement What is already known on this subject? Previous studies have revealed the structure and location of BTG4. BTG4 inhibit cell proliferative, promote apoptosis, induce G1 cell cycle arrest. BTG4 promotes the development of mouse embryos from cell stage 1 to 2. The methylation and biological function of BTG4 were clarified in gastric and/or colorectal cancer cells. What do the results of this study add? BTG4 is found to closely link to reflect the carcinogenesis, histogenesis, aggressive behaviors and prognosis of gynecological cancers, and involved in ligand-receptor interaction, microtubule motor activity, dynein light chain binding, cilium organization, assembly, and movement in endometrial and ovarian cancers. What are the implications of these finding for clinical practice and/or further research? Aberrant BTG4 mRNA expression can be employed as a marker of the tumorigenesis, histogenesis, aggressiveness and prognosis of gynecological cancers in the future practice and guide the investigation of BTG4-related signal pathways.
AbstractList BTG4 arrests the cell cycle and suppresses oocyte and embryonic development. We performed a bioinformatic analysis of BTG4 expression. BTG4 expression was downregulated in breast cancer compared with normal tissues (p < .05), but the opposite was observed in cervical, endometrial and ovarian cancers (p < .05). BTG4 methylation was negatively correlated with its mRNA expression in breast, cervical and endometrial cancers (p < .05). BTG4 mRNA expression was negatively correlated with T staging and distant metastasis of breast cancer; and with tumor invasion, clinical stage, low weight and BMI, low histological grade and no diabetes in endometrial cancer but positively with T stage and non-keratinizing squamous carcinoma in endometrial cancer. BTG4 expression was negatively correlated with the survival of ovarian cancer patients (p < .05), but positively for breast, cervical and endometrial cancers (p < .05). BTG4 expression is thus a potential marker reflecting the carcinogenesis, aggressiveness and prognosis in gynecological cancers.Impact Statement What is already known on this subject? Previous studies have revealed the structure and location of BTG4. BTG4 inhibit cell proliferative, promote apoptosis, induce G1 cell cycle arrest. BTG4 promotes the development of mouse embryos from cell stage 1 to 2. The methylation and biological function of BTG4 were clarified in gastric and/or colorectal cancer cells. What do the results of this study add? BTG4 is found to closely link to reflect the carcinogenesis, histogenesis, aggressive behaviors and prognosis of gynecological cancers, and involved in ligand-receptor interaction, microtubule motor activity, dynein light chain binding, cilium organization, assembly, and movement in endometrial and ovarian cancers. What are the implications of these finding for clinical practice and/or further research? Aberrant BTG4 mRNA expression can be employed as a marker of the tumorigenesis, histogenesis, aggressiveness and prognosis of gynecological cancers in the future practice and guide the investigation of BTG4-related signal pathways.
BTG4 arrests the cell cycle and suppresses oocyte and embryonic development. We performed a bioinformatic analysis of expression. expression was downregulated in breast cancer compared with normal tissues (  < .05), but the opposite was observed in cervical, endometrial and ovarian cancers (  < .05). methylation was negatively correlated with its mRNA expression in breast, cervical and endometrial cancers (  < .05). mRNA expression was negatively correlated with T staging and distant metastasis of breast cancer; and with tumor invasion, clinical stage, low weight and BMI, low histological grade and no diabetes in endometrial cancer but positively with T stage and non-keratinizing squamous carcinoma in endometrial cancer. expression was negatively correlated with the survival of ovarian cancer patients (  < .05), but positively for breast, cervical and endometrial cancers (  < .05). expression is thus a potential marker reflecting the carcinogenesis, aggressiveness and prognosis in gynecological cancers.Impact Statement Previous studies have revealed the structure and location of BTG4. BTG4 inhibit cell proliferative, promote apoptosis, induce G1 cell cycle arrest. BTG4 promotes the development of mouse embryos from cell stage 1 to 2. The methylation and biological function of BTG4 were clarified in gastric and/or colorectal cancer cells. BTG4 is found to closely link to reflect the carcinogenesis, histogenesis, aggressive behaviors and prognosis of gynecological cancers, and involved in ligand-receptor interaction, microtubule motor activity, dynein light chain binding, cilium organization, assembly, and movement in endometrial and ovarian cancers. Aberrant BTG4 mRNA expression can be employed as a marker of the tumorigenesis, histogenesis, aggressiveness and prognosis of gynecological cancers in the future practice and guide the investigation of BTG4-related signal pathways.
BTG4 arrests the cell cycle and suppresses oocyte and embryonic development. We performed a bioinformatic analysis of BTG4 expression. BTG4 expression was downregulated in breast cancer compared with normal tissues (p < .05), but the opposite was observed in cervical, endometrial and ovarian cancers (p < .05). BTG4 methylation was negatively correlated with its mRNA expression in breast, cervical and endometrial cancers (p < .05). BTG4 mRNA expression was negatively correlated with T staging and distant metastasis of breast cancer; and with tumor invasion, clinical stage, low weight and BMI, low histological grade and no diabetes in endometrial cancer but positively with T stage and non-keratinizing squamous carcinoma in endometrial cancer. BTG4 expression was negatively correlated with the survival of ovarian cancer patients (p < .05), but positively for breast, cervical and endometrial cancers (p < .05). BTG4 expression is thus a potential marker reflecting the carcinogenesis, aggressiveness and prognosis in gynecological cancers. Impact Statement What is already known on this subject? Previous studies have revealed the structure and location of BTG4. BTG4 inhibit cell proliferative, promote apoptosis, induce G1 cell cycle arrest. BTG4 promotes the development of mouse embryos from cell stage 1 to 2. The methylation and biological function of BTG4 were clarified in gastric and/or colorectal cancer cells. What do the results of this study add? BTG4 is found to closely link to reflect the carcinogenesis, histogenesis, aggressive behaviors and prognosis of gynecological cancers, and involved in ligand-receptor interaction, microtubule motor activity, dynein light chain binding, cilium organization, assembly, and movement in endometrial and ovarian cancers. What are the implications of these finding for clinical practice and/or further research? Aberrant BTG4 mRNA expression can be employed as a marker of the tumorigenesis, histogenesis, aggressiveness and prognosis of gynecological cancers in the future practice and guide the investigation of BTG4-related signal pathways.
BTG4 arrests the cell cycle and suppresses oocyte and embryonic development. We performed a bioinformatic analysis of BTG4 expression. BTG4 expression was downregulated in breast cancer compared with normal tissues (p < .05), but the opposite was observed in cervical, endometrial and ovarian cancers (p < .05). BTG4 methylation was negatively correlated with its mRNA expression in breast, cervical and endometrial cancers (p < .05). BTG4 mRNA expression was negatively correlated with T staging and distant metastasis of breast cancer; and with tumor invasion, clinical stage, low weight and BMI, low histological grade and no diabetes in endometrial cancer but positively with T stage and non-keratinizing squamous carcinoma in endometrial cancer. BTG4 expression was negatively correlated with the survival of ovarian cancer patients (p < .05), but positively for breast, cervical and endometrial cancers (p < .05). BTG4 expression is thus a potential marker reflecting the carcinogenesis, aggressiveness and prognosis in gynecological cancers.Impact StatementWhat is already known on this subject? Previous studies have revealed the structure and location of BTG4. BTG4 inhibit cell proliferative, promote apoptosis, induce G1 cell cycle arrest. BTG4 promotes the development of mouse embryos from cell stage 1 to 2. The methylation and biological function of BTG4 were clarified in gastric and/or colorectal cancer cells.What do the results of this study add? BTG4 is found to closely link to reflect the carcinogenesis, histogenesis, aggressive behaviors and prognosis of gynecological cancers, and involved in ligand-receptor interaction, microtubule motor activity, dynein light chain binding, cilium organization, assembly, and movement in endometrial and ovarian cancers.What are the implications of these finding for clinical practice and/or further research? Aberrant BTG4 mRNA expression can be employed as a marker of the tumorigenesis, histogenesis, aggressiveness and prognosis of gynecological cancers in the future practice and guide the investigation of BTG4-related signal pathways.BTG4 arrests the cell cycle and suppresses oocyte and embryonic development. We performed a bioinformatic analysis of BTG4 expression. BTG4 expression was downregulated in breast cancer compared with normal tissues (p < .05), but the opposite was observed in cervical, endometrial and ovarian cancers (p < .05). BTG4 methylation was negatively correlated with its mRNA expression in breast, cervical and endometrial cancers (p < .05). BTG4 mRNA expression was negatively correlated with T staging and distant metastasis of breast cancer; and with tumor invasion, clinical stage, low weight and BMI, low histological grade and no diabetes in endometrial cancer but positively with T stage and non-keratinizing squamous carcinoma in endometrial cancer. BTG4 expression was negatively correlated with the survival of ovarian cancer patients (p < .05), but positively for breast, cervical and endometrial cancers (p < .05). BTG4 expression is thus a potential marker reflecting the carcinogenesis, aggressiveness and prognosis in gynecological cancers.Impact StatementWhat is already known on this subject? Previous studies have revealed the structure and location of BTG4. BTG4 inhibit cell proliferative, promote apoptosis, induce G1 cell cycle arrest. BTG4 promotes the development of mouse embryos from cell stage 1 to 2. The methylation and biological function of BTG4 were clarified in gastric and/or colorectal cancer cells.What do the results of this study add? BTG4 is found to closely link to reflect the carcinogenesis, histogenesis, aggressive behaviors and prognosis of gynecological cancers, and involved in ligand-receptor interaction, microtubule motor activity, dynein light chain binding, cilium organization, assembly, and movement in endometrial and ovarian cancers.What are the implications of these finding for clinical practice and/or further research? Aberrant BTG4 mRNA expression can be employed as a marker of the tumorigenesis, histogenesis, aggressiveness and prognosis of gynecological cancers in the future practice and guide the investigation of BTG4-related signal pathways.
BTG4 arrests the cell cycle and suppresses oocyte and embryonic development. We performed a bioinformatic analysis of BTG4 expression. BTG4 expression was downregulated in breast cancer compared with normal tissues (p < .05), but the opposite was observed in cervical, endometrial and ovarian cancers (p < .05). BTG4 methylation was negatively correlated with its mRNA expression in breast, cervical and endometrial cancers (p < .05). BTG4 mRNA expression was negatively correlated with T staging and distant metastasis of breast cancer; and with tumor invasion, clinical stage, low weight and BMI, low histological grade and no diabetes in endometrial cancer but positively with T stage and non-keratinizing squamous carcinoma in endometrial cancer. BTG4 expression was negatively correlated with the survival of ovarian cancer patients (p < .05), but positively for breast, cervical and endometrial cancers (p < .05). BTG4 expression is thus a potential marker reflecting the carcinogenesis, aggressiveness and prognosis in gynecological cancers.Impact StatementWhat is already known on this subject? Previous studies have revealed the structure and location of BTG4. BTG4 inhibit cell proliferative, promote apoptosis, induce G1 cell cycle arrest. BTG4 promotes the development of mouse embryos from cell stage 1 to 2. The methylation and biological function of BTG4 were clarified in gastric and/or colorectal cancer cells.What do the results of this study add? BTG4 is found to closely link to reflect the carcinogenesis, histogenesis, aggressive behaviors and prognosis of gynecological cancers, and involved in ligand-receptor interaction, microtubule motor activity, dynein light chain binding, cilium organization, assembly, and movement in endometrial and ovarian cancers.What are the implications of these finding for clinical practice and/or further research? Aberrant BTG4 mRNA expression can be employed as a marker of the tumorigenesis, histogenesis, aggressiveness and prognosis of gynecological cancers in the future practice and guide the investigation of BTG4-related signal pathways.
Author Xue, Hang
Zheng, Hua-chuan
Zhang, Cong-yu
Zhang, Rui
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  surname: Zhang
  fullname: Zhang, Rui
  organization: Department of Colorectal Surgery, Liaoning Cancer Hospital
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CitedBy_id crossref_primary_10_1080_01443615_2023_2216280
crossref_primary_10_1080_01443615_2023_2228899
crossref_primary_10_3390_antiox13121567
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Issue 1
Keywords BTG4
carcinogenesis
bioinformatic analysis
prognosis
aggressiveness
gynecological cancer
Language English
License open-access: http://creativecommons.org/licenses/by/4.0/: This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Snippet BTG4 arrests the cell cycle and suppresses oocyte and embryonic development. We performed a bioinformatic analysis of BTG4 expression. BTG4 expression was...
BTG4 arrests the cell cycle and suppresses oocyte and embryonic development. We performed a bioinformatic analysis of expression. expression was downregulated...
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StartPage 2182672
SubjectTerms aggressiveness
Animals
bioinformatic analysis
Breast cancer
BTG4
Carcinogenesis
Cell cycle
Cell Cycle Proteins
Colorectal cancer
Computational Biology
Endometrial cancer
Endometrial Neoplasms
Female
Gynecological cancer
Humans
Medical prognosis
Mice
Ovarian cancer
Ovarian Neoplasms - genetics
Pregnancy
Prognosis
RNA, Messenger
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Title Bioinformatic analysis of the clinicopathological and prognostic significance of oocyte-arresting BTG4 mRNA expression in gynecological cancers
URI https://www.tandfonline.com/doi/abs/10.1080/01443615.2023.2182672
https://www.ncbi.nlm.nih.gov/pubmed/36880525
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Volume 43
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