Estrogen promotes fat mass and obesity-associated protein nuclear localization and enhances endometrial cancer cell proliferation via the mTOR signaling pathway

Zhu, Yue; Shen, Jiaqi; Gao, Liyan; Yan, Feng

doi:10.3892/or.2016.4613

Cited by 51 publications

(45 citation statements)

References 32 publications

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“…Zhu et al report that the clinical outcome of EC is influenced by the expression of fat mass and the obesity-associated gene (FTO). Using immunohistochemistry and Western blotting, they observed that obese women with endometrial cancer showed estrogen (ERα-dependent)-induced FTO nuclear accumulation in the mTOR signaling pathway, which contributed to worse clinical outcomes [33].…”

Section: Metabolic Impact On Carcinogenesis By Mtormentioning

confidence: 99%

The Communication between the PI3K/AKT/mTOR Pathway and Y-Box Binding Protein-1 in Gynecological Cancer

Sobočan

Bračič

Knez

et al. 2020

Cancers

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Studies of the mechanistic (mammalian) target of rapamycin inhibitors (mTOR) represent a step towards the targeted treatment of gynecological cancers. It has been shown that women with increased levels of mTOR signaling pathway targets have worse prognosis compared to women with normal mTOR levels. Yet, targeting mTOR alone has led to unsatisfactory outcomes in gynecological cancer. The aim of our review was therefore to provide an overview of the most recent clinical results and basic findings on the interplay of mTOR signaling and cold shock proteins in gynecological malignancies. Due to their oncogenic activity, there are promising data showing that mTOR and Y-box-protein 1 (YB-1) dual targeting improves the inhibition of carcinogenic activity. Although several components differentially expressed in patients with ovarian, endometrial, and cervical cancer of the mTOR were identified, there are only a few investigated downstream actors in gynecological cancer connecting them with YB-1. Our analysis shows that YB-1 is an important player impacting AKT as well as the downstream actors interacting with mTOR such as epidermal growth factor receptor (EGFR), Snail or E-cadherin.

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Section: Metabolic Impact On Carcinogenesis By Mtormentioning

confidence: 99%

The Communication between the PI3K/AKT/mTOR Pathway and Y-Box Binding Protein-1 in Gynecological Cancer

Sobočan

Bračič

Knez

et al. 2020

Cancers

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“…The expression of FTO mRNA is extensive in different human tissues indicates that it may be involved in important biological processes (11,12). Although obesity is a basic biological mechanism of the risk of the development of cancer it is not fully understood, recent studies have shown that the FTO gene may associate with cancer risk (13), such as breast (14), thyroid (15) and endometrial cancer (16).…”

Section: Introductionmentioning

confidence: 99%

FTO expression is associated with the occurrence of gastric cancer and prognosis

et al. 2017

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Fat mass and obesity associated (FTO) is a protein-coding gene. FTO gene is an obesity related gene, also known as the obesity gene. It has been reported previously that FTO is associated with a variety of malignant cancers, such as breast, thyroid and endometrial cancer. The aim of the present study was investigate the FTO expression of human gastric cancer and to investigate its clinical value. FTO expression was determined by immunohistochemical analysis with tissue microarrays in GC tissues and corresponding adjacent non-tumor tissues. Moreover, the results in protein and mRNA level were confirmed by the real-time PCR and western blot analysis. The relationship between the FTO expression and the pathological characteristics of GC patients was also explored. In addition, by using MTT, clone formation and transwell assays, we studied the effects of FTO expression on biological function of GC cells in vitro. The Kaplan-Meier method and the log-rank test were used to compare the overall survival rate between the FTO high-expression group and the low-expression group. We affirmed repeatedly upregulation of FTO expression in both protein and mRNA levels in GC tissues compared to corresponding adjacent non-tumor tissues. Immunohistochemistry by tissue microarray of FTO expression was remarkably increased in GC tissues (72 of 128, 56.3%) compared with adjacent non-tumor tissues (24 of 62, 38.7%). FTO expression level was closely related to low differentiation (P<0.001), lymph node metastasis (P=0.029). The expression of FTO was positively correlated with TNM stage (P<0.001). the Kaplan-Meier analysis showed that high FTO expression was significantly associated with poor prognosis in GC patients. Downregulation of FTO expression significantly inhibited the proliferation, migration and invasion of GC cell lines. On the contrary, overexpression of FTO promoted the proliferation, migration and invasion of GC cell lines. This study indicates that FTO expression may have an important role in promoting the occurrence of GC, and it may be an vital molecular marker in the diagnosis and prognosis of GC patients.

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“…13,14 Alternation of these component genes in the methyltransferase complex can give rise to a significant phenotype change, such as carcinogenesis. [15][16][17][18][19][20][21] FTO, the first identified "eraser" of m 6 A, has been reported to play an oncogenic role in various types of cancer, including endometrial, 22 breast, 23 pancreatic cancer, 24 and acute myeloid leukemia (AML), 25 suggesting the functional importance of the mRNA m 6 A methylation and its modulators in cancer. Nonetheless, FTO or m 6 A methylation profiles and functions in the regulation of chemo-radiotherapy resistance have rarely been investigated and prompted us to investigate the role and underlying mechanisms of the FTO or m 6 A in CSCC chemo-radiotherapy resistance regulation.…”

mentioning

confidence: 99%

FTO regulates the chemo‐radiotherapy resistance of cervical squamous cell carcinoma (CSCC) by targeting β‐catenin through mRNA demethylation

Zhou

Bai

Xia

et al. 2018

Molecular Carcinogenesis

301

228

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The role of N -methyladenosine (m A) demethylase fat mass and obesity-associated protein (FTO) in the regulation of chemo-radiotherapy resistance remains largely unknown. Here, we show that the mRNA level of FTO is elevated in cervical squamous cell carcinoma (CSCC) tissues when compared with respective adjacent normal tissues. FTO enhances the chemo-radiotherapy resistance both in vitro and in vivo through regulating expression of β-catenin by reducing m A levels in its mRNA transcripts and in turn increases excision repair cross-complementation group 1 (ERCC1) activity. Clinically, the prognostic value of FTO for overall survival is found to be dependent on β-catenin expression in human CSCC samples. Taken together, these findings uncover a critical function for FTO and its substrate m A in the regulation of chemo-radiotherapy resistance, which may bear potential clinical implications for CSCC treatment.

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Estrogen promotes fat mass and obesity-associated protein nuclear localization and enhances endometrial cancer cell proliferation via the mTOR signaling pathway

Cited by 51 publications

References 32 publications

The Communication between the PI3K/AKT/mTOR Pathway and Y-Box Binding Protein-1 in Gynecological Cancer

The Communication between the PI3K/AKT/mTOR Pathway and Y-Box Binding Protein-1 in Gynecological Cancer

FTO expression is associated with the occurrence of gastric cancer and prognosis

FTO regulates the chemo‐radiotherapy resistance of cervical squamous cell carcinoma (CSCC) by targeting β‐catenin through mRNA demethylation

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