Hormonal contraception and risk of endometrial cancer: a systematic review

Mueck, Alfred O.; Seeger, Harald; Rabe, T.

doi:10.1677/erc-10-0076

Cited by 85 publications

(48 citation statements)

References 48 publications

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“…Two different clinicopathological subtypes of endometrial cancer are recognized: one is estrogen-related type 1 (endometroid), and the other is non-estrogen-related type 2 (non-endometroid such as papillary serous and clear cell) (1). Although various endocrine, genetic and external factors, such as unopposed estrogen exposure, complex hyperplasia with atypia, and treatment with tamoxifen during breast cancer therapy, may contribute to its initiation and progression, the etiology of endometrial carcinoma remains not fully understood (2).…”

Section: Introductionmentioning

confidence: 99%

microRNA-30c negatively regulates endometrial cancer cells by targeting metastasis-associated gene-1

Zhou

Xu²,

Xun³

et al. 2011

Oncol Rep

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Abstract.It is well known that microRNAs (miRNAs) play important roles in cancer development by targeting oncogenes or tumor-suppressor genes. However, little is known regarding the mechanisms of miR-30c action in endometrial cancer. In this study, we aimed to determine whether miR-30c targets metastasis-associated gene-1 (MTA1) and acts as a tumor suppressor in endometrial cancer cell lines Ishikawa (estrogen receptor-positive, ER + ) and HEC-1-B (ER -) by down-regulating MTA1. As a result, in both Ishikawa and HEC-1-B cells, realtime PCR demonstrated that overexpression of miR-30c led to the down-regulation of MTA1 mRNA (P<0.05), while Western blotting confirmed the reduced expression levels of MTA1 protein (P<0.01). A dual-luciferase reporter assay demonstrated that miR-30c was directly bound to the 3'-untranslated regions of MTA1. Then we studied the biological mechanisms of endometrial cancer cells transfected with the Pre-miR-30c plasmid. MTT assay and growth curves revealed that miR-30c inhibits both Ishikawa and HEC-1-B cell proliferation. However, we did not see obvious differences in rates of apoptosis between miR30c-overexpressing and the negative control cells. Then using wound-healing and Matrigel invasion assays, we found that the migratory and invasive abilities of cells transfected with the Pre-miR-30c plasmid were significantly suppressed compared with the control cells (P<0.01). Overall, our study, for the first time, showed that MTA1 is negatively regulated by miR-30c and that overexpression of miR-30c inhibits the proliferative, migratory and invasive abilities of endometrial cancer cells. These results suggest that miR-30c acts as a tumor suppressor and negatively regulates endometrial cancer cells by targeting MTA1. IntroductionEndometrial carcinoma is a common worldwide gynecologic malignancy. Two different clinicopathological subtypes of endometrial cancer are recognized: one is estrogen-related type 1 (endometroid), and the other is non-estrogen-related type 2 (non-endometroid such as papillary serous and clear cell) (1). Although various endocrine, genetic and external factors, such as unopposed estrogen exposure, complex hyperplasia with atypia, and treatment with tamoxifen during breast cancer therapy, may contribute to its initiation and progression, the etiology of endometrial carcinoma remains not fully understood (2). The primary and most effective treatment for patients with localized disease is still hysterectomy and bilateral salpingo-oophorectomy (3). Although adjuvant radiotherapy and chemotherapy may reduce local recurrence and systemic metastases, the associated toxicity and morbidity are significant (4). Thus, the search for novel molecular targets as therapeutic agents through an increased understanding of the molecular mechanisms of endometrial tumorigenesis is in urgent need. microRNAs (miRNAs) are a class of conserved short (19-25 nt) RNAs that regulate gene expression through basepairing with the 3'-untranslated regions (3'-UTR) of target mRNAs (5) and play an importa...

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Section: Introductionmentioning

confidence: 99%

microRNA-30c negatively regulates endometrial cancer cells by targeting metastasis-associated gene-1

Zhou

Xu²,

Xun³

et al. 2011

Oncol Rep

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“…Mueck et al 24 recently published a review of all studies of the relationship between endometrial cancer and hormonal contraception. More than 15 case-control studies and at least four large cohort studies demonstrated a decrease in the risk of endometrial cancer of about 50% if COCs had ever been used.…”

Section: Endometrial Cancermentioning

confidence: 99%

Non-contraceptive benefits of oral contraceptives

Dhont¹

2011

OAJC

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Abstract:The health benefits of the oral contraceptive (OC) pill are numerous and outweigh the risks of OC use. There are unintended but useful preventive side effects and potential therapeutic uses of OCs apart from contraception itself. Unequivocal evidence for the protective influence of combined OCs against ovarian and endometrial cancers, and colon cancer to a lesser extent, has been found. The pill also reduces the incidence of benign breast disease, functional ovarian cysts, pelvic inflammatory disease requiring hospitalization, ectopic pregnancy, and irondeficiency anemia. The pill can be used for the treatment of several gynecologic disorders such as dysmenorrhea, irregular or excessive bleeding, acne, hirsutism, and endometriosis-associated pain, whether prescribed solely to treat these symptoms or prescribed to treat them in addition to providing contraception. These health benefits are often underestimated, as they get too little attention from the mass media.

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“…Endometrial cancer is the most common gynecologic malignancy, and its occurrence is related to both endogenous and exogenous hormone exposures (1)(2)(3)(4). Combination oral contraceptives (COC) and menopausal hormone therapy are the most common forms of exogenous hormones.…”

Section: Introductionmentioning

confidence: 99%

Hormone Contraception before the First Birth and Endometrial Cancer Risk

Cook¹,

Dong²,

Round³

et al. 2014

Cancer Epidemiology, Biomarkers &Amp; Prevention

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There is a well-documented reduction in endometrial cancer risk with combined oral contraceptive (COC) use. COC use before the first full-term pregnancy may affect breast cancer risk for decades, but this relationship has not been investigated in endometrial cancer. We investigated the risk for endometrial cancer with COC use before the first full-term pregnancy. Cases (n ¼ 524) from a population-based cancer registry and age-matched controls (n ¼ 1,032) were recruited between 2002 and 2006 in Alberta, Canada. Participants completed an inperson interview and provided detailed information on exogenous hormone use and other risk factors. Risk reductions in endometrial cancer with COC use over the premenopausal years were consistent with the published literature. We also found evidence of a long-term, significant risk reduction in parous women with COC use before the first full-term pregnancy. Among parous women, 5 years of COC use before a first fullterm pregnancy was associated with a significant reduction in risk [adjusted OR, 0.42

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Hormonal contraception and risk of endometrial cancer: a systematic review

Cited by 85 publications

References 48 publications

microRNA-30c negatively regulates endometrial cancer cells by targeting metastasis-associated gene-1

microRNA-30c negatively regulates endometrial cancer cells by targeting metastasis-associated gene-1

Non-contraceptive benefits of oral contraceptives

Hormone Contraception before the First Birth and Endometrial Cancer Risk

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