Cellular models of development of ovarian high‐grade serous carcinoma: A review of cell of origin and mechanisms of carcinogenesis

High‐grade serous carcinoma (HGSC) is the most common and malignant histological type of epithelial ovarian cancer, the origin of which remains controversial. Currently, the secretory epithelial cells of the fallopian tube are regarded as the main origin and the ovarian surface epithelial cells as a...

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Published inCell proliferation Vol. 54; no. 5; pp. e13029 - n/a
Main Authors Mei, Jie, Tian, Huixiang, Huang, Hsuan‐Shun, Hsu, Che‐Fang, Liou, Yuligh, Wu, Nayiyuan, Zhang, Wei, Chu, Tang‐Yuan
Format Journal Article
LanguageEnglish
Published England John Wiley & Sons, Inc 01.05.2021
John Wiley and Sons Inc
Subjects
Animals
Birth control
Cancer
Carcinogenesis
Carcinogens
Carcinoma - metabolism
Carcinoma - pathology
Cell culture
Cell Transformation, Neoplastic
Cyclin-dependent kinase 4
DNA damage
Enzymes
Epithelial cells
Epithelium
Fallopian tube
Fallopian tubes
Fallopian Tubes - cytology
Fallopian Tubes - metabolism
Fallopian Tubes - pathology
Female
Follicular fluid
Genetic transformation
Genomic instability
Growth factors
Humans
Hypotheses
Immortalization
Insulin-like growth factors
Menstruation
Models, Biological
Mutation
Ovarian cancer
Ovarian carcinoma
Ovarian Neoplasms - metabolism
Ovarian Neoplasms - pathology
Ovaries
Ovulation
Peritoneum
Pregnancy
Proteins
Review
Reviews
Telomerase - genetics
Telomerase - metabolism
Telomerase reverse transcriptase
Transformations
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Protein p53 - metabolism
Yes-associated protein
Online AccessGet full text

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Abstract High‐grade serous carcinoma (HGSC) is the most common and malignant histological type of epithelial ovarian cancer, the origin of which remains controversial. Currently, the secretory epithelial cells of the fallopian tube are regarded as the main origin and the ovarian surface epithelial cells as a minor origin. In tubal epithelium, these cells acquire TP53 mutations and expand to a morphologically normal ‘p53 signature’ lesion, transform to serous tubal intraepithelial carcinoma and metastasize to the ovaries and peritoneum where they develop into HGSC. This shifting paradigm of the main cell of origin has revolutionarily changed the focus of HGSC research. Various cell lines have been derived from the two cellular origins by acquiring immortalization via overexpression of hTERT plus disruption of TP53 and the CDK4/RB pathway. Malignant transformation was achieved by adding canonical driver mutations (such as gain of CCNE1) revealed by The Cancer Genome Atlas or by noncanonical gain of YAP and miR181a. Alternatively, because of the extreme chromosomal instability, spontaneous transformation can be achieved by long passage of murine immortalized cells, whereas in humans, it requires ovulatory follicular fluid, containing regenerating growth factors to facilitate spontaneous transformation. These artificially and spontaneously transformed cell systems in both humans and mice have been widely used to discover carcinogens, oncogenic pathways and malignant behaviours in the development of HGSC. Here, we review the origin, aetiology and carcinogenic mechanism of HGSC and comprehensively summarize the cell models used to study this fatal cancer having multiple cells of origin and overt genomic instability. The genetic alterations and known mechanism of transformation by ovulation and retrograde menstruation in the development of HGSC from the FTE.
AbstractList High-grade serous carcinoma (HGSC) is the most common and malignant histological type of epithelial ovarian cancer, the origin of which remains controversial. Currently, the secretory epithelial cells of the fallopian tube are regarded as the main origin and the ovarian surface epithelial cells as a minor origin. In tubal epithelium, these cells acquire TP53 mutations and expand to a morphologically normal 'p53 signature' lesion, transform to serous tubal intraepithelial carcinoma and metastasize to the ovaries and peritoneum where they develop into HGSC. This shifting paradigm of the main cell of origin has revolutionarily changed the focus of HGSC research. Various cell lines have been derived from the two cellular origins by acquiring immortalization via overexpression of hTERT plus disruption of TP53 and the CDK4/RB pathway. Malignant transformation was achieved by adding canonical driver mutations (such as gain of CCNE1) revealed by The Cancer Genome Atlas or by noncanonical gain of YAP and miR181a. Alternatively, because of the extreme chromosomal instability, spontaneous transformation can be achieved by long passage of murine immortalized cells, whereas in humans, it requires ovulatory follicular fluid, containing regenerating growth factors to facilitate spontaneous transformation. These artificially and spontaneously transformed cell systems in both humans and mice have been widely used to discover carcinogens, oncogenic pathways and malignant behaviours in the development of HGSC. Here, we review the origin, aetiology and carcinogenic mechanism of HGSC and comprehensively summarize the cell models used to study this fatal cancer having multiple cells of origin and overt genomic instability.High-grade serous carcinoma (HGSC) is the most common and malignant histological type of epithelial ovarian cancer, the origin of which remains controversial. Currently, the secretory epithelial cells of the fallopian tube are regarded as the main origin and the ovarian surface epithelial cells as a minor origin. In tubal epithelium, these cells acquire TP53 mutations and expand to a morphologically normal 'p53 signature' lesion, transform to serous tubal intraepithelial carcinoma and metastasize to the ovaries and peritoneum where they develop into HGSC. This shifting paradigm of the main cell of origin has revolutionarily changed the focus of HGSC research. Various cell lines have been derived from the two cellular origins by acquiring immortalization via overexpression of hTERT plus disruption of TP53 and the CDK4/RB pathway. Malignant transformation was achieved by adding canonical driver mutations (such as gain of CCNE1) revealed by The Cancer Genome Atlas or by noncanonical gain of YAP and miR181a. Alternatively, because of the extreme chromosomal instability, spontaneous transformation can be achieved by long passage of murine immortalized cells, whereas in humans, it requires ovulatory follicular fluid, containing regenerating growth factors to facilitate spontaneous transformation. These artificially and spontaneously transformed cell systems in both humans and mice have been widely used to discover carcinogens, oncogenic pathways and malignant behaviours in the development of HGSC. Here, we review the origin, aetiology and carcinogenic mechanism of HGSC and comprehensively summarize the cell models used to study this fatal cancer having multiple cells of origin and overt genomic instability.
High‐grade serous carcinoma (HGSC) is the most common and malignant histological type of epithelial ovarian cancer, the origin of which remains controversial. Currently, the secretory epithelial cells of the fallopian tube are regarded as the main origin and the ovarian surface epithelial cells as a minor origin. In tubal epithelium, these cells acquire TP53 mutations and expand to a morphologically normal ‘p53 signature’ lesion, transform to serous tubal intraepithelial carcinoma and metastasize to the ovaries and peritoneum where they develop into HGSC. This shifting paradigm of the main cell of origin has revolutionarily changed the focus of HGSC research. Various cell lines have been derived from the two cellular origins by acquiring immortalization via overexpression of hTERT plus disruption of TP53 and the CDK4/RB pathway. Malignant transformation was achieved by adding canonical driver mutations (such as gain of CCNE1) revealed by The Cancer Genome Atlas or by noncanonical gain of YAP and miR181a. Alternatively, because of the extreme chromosomal instability, spontaneous transformation can be achieved by long passage of murine immortalized cells, whereas in humans, it requires ovulatory follicular fluid, containing regenerating growth factors to facilitate spontaneous transformation. These artificially and spontaneously transformed cell systems in both humans and mice have been widely used to discover carcinogens, oncogenic pathways and malignant behaviours in the development of HGSC. Here, we review the origin, aetiology and carcinogenic mechanism of HGSC and comprehensively summarize the cell models used to study this fatal cancer having multiple cells of origin and overt genomic instability. The genetic alterations and known mechanism of transformation by ovulation and retrograde menstruation in the development of HGSC from the FTE.
High‐grade serous carcinoma (HGSC) is the most common and malignant histological type of epithelial ovarian cancer, the origin of which remains controversial. Currently, the secretory epithelial cells of the fallopian tube are regarded as the main origin and the ovarian surface epithelial cells as a minor origin. In tubal epithelium, these cells acquire TP53 mutations and expand to a morphologically normal ‘p53 signature’ lesion, transform to serous tubal intraepithelial carcinoma and metastasize to the ovaries and peritoneum where they develop into HGSC. This shifting paradigm of the main cell of origin has revolutionarily changed the focus of HGSC research. Various cell lines have been derived from the two cellular origins by acquiring immortalization via overexpression of hTERT plus disruption of TP53 and the CDK4/RB pathway. Malignant transformation was achieved by adding canonical driver mutations (such as gain of CCNE1) revealed by The Cancer Genome Atlas or by noncanonical gain of YAP and miR181a. Alternatively, because of the extreme chromosomal instability, spontaneous transformation can be achieved by long passage of murine immortalized cells, whereas in humans, it requires ovulatory follicular fluid, containing regenerating growth factors to facilitate spontaneous transformation. These artificially and spontaneously transformed cell systems in both humans and mice have been widely used to discover carcinogens, oncogenic pathways and malignant behaviours in the development of HGSC. Here, we review the origin, aetiology and carcinogenic mechanism of HGSC and comprehensively summarize the cell models used to study this fatal cancer having multiple cells of origin and overt genomic instability.
Author Liou, Yuligh
Zhang, Wei
Huang, Hsuan‐Shun
Mei, Jie
Chu, Tang‐Yuan
Wu, Nayiyuan
Tian, Huixiang
Hsu, Che‐Fang
AuthorAffiliation 3 Engineering Research Center of Applied Technology of Pharmacogenomics Ministry of Education Changsha China
4 National Clinical Research Center for Geriatric Disorders Changsha China
7 Hunan Cancer Hospital The Affiliated Cancer Hospital of Xiangya School of Medicine Central South University Hunan China
1 Department of Clinical Pharmacology Xiangya Hospital Central South University Changsha China
8 Department of Obstetrics & Gynecology Buddhist Tzu Chi General Hospital Hualien Taiwan, ROC
2 Institute of Clinical Pharmacology Hunan Key Laboratory of Pharmacogenetics Central South University Changsha China
6 Center for Prevention and Therapy of Gynecological Cancers Department of Research Buddhist Tzu Chi General Hospital Hualien Taiwan, ROC
9 Department of Life Sciences Tzu Chi University Hualien Taiwan, ROC
5 Department of Pharmacy Xiangya Hospital Central South University Changsha China
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– name: 3 Engineering Research Center of Applied Technology of Pharmacogenomics Ministry of Education Changsha China
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/33768671$$D View this record in MEDLINE/PubMed
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2021 The Authors. Cell Proliferation Published by John Wiley & Sons Ltd.
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This research was supported by the National Natural Science Foundation of China (grant number 81874329, 82073945).
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Snippet High‐grade serous carcinoma (HGSC) is the most common and malignant histological type of epithelial ovarian cancer, the origin of which remains controversial....
High-grade serous carcinoma (HGSC) is the most common and malignant histological type of epithelial ovarian cancer, the origin of which remains controversial....
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SubjectTerms Animals
Birth control
Cancer
Carcinogenesis
Carcinogens
Carcinoma - metabolism
Carcinoma - pathology
Cell culture
Cell Transformation, Neoplastic
Cyclin-dependent kinase 4
DNA damage
Enzymes
Epithelial cells
Epithelium
Fallopian tube
Fallopian tubes
Fallopian Tubes - cytology
Fallopian Tubes - metabolism
Fallopian Tubes - pathology
Female
Follicular fluid
Genetic transformation
Genomic instability
Growth factors
Humans
Hypotheses
Immortalization
Insulin-like growth factors
Menstruation
Models, Biological
Mutation
Ovarian cancer
Ovarian carcinoma
Ovarian Neoplasms - metabolism
Ovarian Neoplasms - pathology
Ovaries
Ovulation
Peritoneum
Pregnancy
Proteins
Review
Reviews
Telomerase - genetics
Telomerase - metabolism
Telomerase reverse transcriptase
Transformations
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Protein p53 - metabolism
Yes-associated protein
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Title Cellular models of development of ovarian high‐grade serous carcinoma: A review of cell of origin and mechanisms of carcinogenesis
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