Bisphenol A induces human uterine leiomyoma cell proliferation through membrane-associated ERα36 via nongenomic signaling pathways

Yu, Linda Chia‐Hui; Das, Piw; Vall, Alejandra J.; Yan, Yuchao; Gao, Xioahua; Sifre, Maria I.; Bortner, Carl D.; Castro, Lysandra; Kissling, Grace E.; Moore, Alicia B.; Dixon, Darlene

doi:10.1016/j.mce.2019.01.001

Cited by 33 publications

(12 citation statements)

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“…These receptors are associated with mitochondrial proteins and considered to be nongenomic signals with pivotal functions. Bisphenol A induced UL cell proliferation through ERα36 as a nongenomic signaling pathway ( 33 ).…”

Section: Discussionmentioning

confidence: 99%

LncRNA APTR Promotes Uterine Leiomyoma Cell Proliferation by Targeting ERα to Activate the Wnt/β-Catenin Pathway

Zhou

Wang

et al. 2021

Front. Oncol.

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The molecular mechanisms by which uterine leiomyoma (UL) cells proliferate are unclear. Long noncoding RNA (lncRNA) is reported to participate in the occurrence and development of gynecological cancers. We investigated the molecular mechanisms that lncRNA uses in UL. We found that lncRNA Alu-mediated p21 transcriptional regulator (APTR) showed higher expression in UL tumor tissues compared with that in normal uterine tissues. APTR induced cell proliferation and colony formation both in vitro and in vivo. The JASPAR database showed that APTR was likely interacted with ERα, and these molecules were identified via laser scanning confocal microscopy and RNA immunoprecipitation analysis. To verify the correlation between APTR and ERα, we overexpressed and underexpressed APTR and simultaneously expressed ERα. The results showed that APTR function was suppressed. APTR increased the expressions of the proteins in the Wnt pathway, and inhibiting ERα eliminated these responses. In conclusion, our data suggest that APTR promoted leiomyoma cell proliferation through the Wnt pathway by targeting ERα, suggesting a new role of APTR in the Wnt signaling pathway in UL.

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Section: Discussionmentioning

confidence: 99%

LncRNA APTR Promotes Uterine Leiomyoma Cell Proliferation by Targeting ERα to Activate the Wnt/β-Catenin Pathway

Zhou

Wang

et al. 2021

Front. Oncol.

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“…5 Uterine fibroids, benign tumors of the uterine muscle, may be influenced by environmental exposures as epidemiologic and laboratory studies indicate that EDCs and metals could play a role. [21][22][23][40][41][42] Compared to white women, African American women have earlier onset of fibroids and worse symptomatology, resulting in an increased risk of pregnancy bleeding and Caesarean delivery. 45 Air pollution has been directly associated with reduced fertility.…”

Section: Environmental Factors In Maternal Health Subfertility Pregnancy Complications and Maternal Morbiditymentioning

confidence: 99%

Environmental Factors Involved in Maternal Morbidity and Mortality

Boyles

Beverly

Fenton

et al. 2021

Journal of Women's Health

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Nongenetic, environmental factors contribute to maternal morbidity and mortality through chemical exposures via air, water, soil, food, and consumer products. Pregnancy represents a particularly sensitive window of susceptibility during which physiological changes to every major organ system increase sensitivity to chemicals that can impact a woman's long-term health. Nonchemical stressors, such as low socioeconomic status, may exacerbate the effects of chemical exposures on maternal health. Racial/ethnic minorities are exposed disproportionately to both chemicals and nonchemical stressors, which likely contribute to the observed health disparities for maternal morbidities and mortality. Epidemiological studies linking exposures to adverse maternal health outcomes underscore the importance of environmental health impacts, and mechanistic studies in model systems reveal how chemicals perturb biological pathways and processes. Environmental stressors are associated with a variety of immediate maternal health impacts, including hypertensive disorders of pregnancy, fibroids, and infertility, as well as long-term maternal health impacts, such as higher risk of breast cancer and metabolic disorders. Identifying and reducing a pregnant woman's environmental exposures is not only beneficial to her offspring but also important to preserve her short-and long-term health.

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“…At environmentally relevant doses, BPA enhanced cell proliferation, induced cyclooxygenase-2 (COX-2) gene expression, and promoted cell migration and invasiveness [57]. BPA induced proliferation in immortalized human UF cells through membrane-associated ERα36 by the activation of Src, epidermal growth factor receptor, Ras, and microtubule affinity regulating kinase pathways [58]. Most of these in vitro studies indicated that BPA increased the proliferation of human UF cells, possibly contributing to UF growth.…”

Section: Bisphenol Amentioning

confidence: 99%

Nonpersistent endocrine disrupting chemicals and reproductive health of women

et al. 2020

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Nonpersistent endocrine disrupting chemicals (npEDCs) are exogenous chemicals or mixtures of industrial agents that can interfere with the normal action of hormone with a shorter half-life and lower liposolubility. These are commonly found in plastics, medical equipment, detergents, and cosmetics. Recently, role of npEDCs on the changes of ovary and/or uterus development and alterations in hormonal signaling has been emphasized. However, many controversial results exist on the effects of npEDCs and reproductive health of women. Thus, we have focused to review the scientific evidence of a causal relationship between exposure to npEDCs and representative female reproductive issues such as menstrual cycle, endometriosis, uterine fibroids, polycystic ovarian syndrome and infertility/subfertility. Though not all studies indicated a positive correlation of npEDCs with female reproductive issues, the reviewed data illustrated that the majority of the available data strengthen the evidence of reproductive health-related actions of npEDCs. In future, recommendations should be made in order to reduce human exposure to npEDCs and to protect from steadily increasing reproductive health risks.

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Bisphenol A induces human uterine leiomyoma cell proliferation through membrane-associated ERα36 via nongenomic signaling pathways

Cited by 33 publications

References 50 publications

LncRNA APTR Promotes Uterine Leiomyoma Cell Proliferation by Targeting ERα to Activate the Wnt/β-Catenin Pathway

LncRNA APTR Promotes Uterine Leiomyoma Cell Proliferation by Targeting ERα to Activate the Wnt/β-Catenin Pathway

Environmental Factors Involved in Maternal Morbidity and Mortality

Nonpersistent endocrine disrupting chemicals and reproductive health of women

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