FEAT expression correlates with tumor size, PR status, HER2 expression, Ki67 index, and molecular subtype and predicts recurrence in breast cancer

Sm, Wang; M, Ye; Zhou, Jingyang; Sm, Ni; Qc, Wei

doi:10.4149/neo_2017_115

Cited by 6 publications

(5 citation statements)

References 22 publications

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“…On the other hand, the current research has deeply explored the viability of using mRNA expression profiles for predicting cancer or discriminating between cancer subtypes. For instance, FEAT, a protein encoded by the METTL13 (methyltransferase like 13) gene, correlates with tumor size in BC (Wang, Ye, Zhou, Ni, & Wei, ). Also, CIZ1b, the b‐variant form of CIZ1 (CIZ1b) is sensitive for the identification of LC patients at stage 1 (Coverley et al, ).…”

Section: Potential Clinical Application Of Tmem88 In Cancermentioning

confidence: 99%

New advances of TMEM88 in cancer initiation and progression, with special emphasis on Wnt signaling pathway

Wang

et al. 2017

Journal Cellular Physiology

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Transmembrane protein 88 (TMEM88), a newly discovered protein localized on the cell membrane.Recent studies showed that TMEM88 was involved in the regulation of several types of cancer.TMEM88 was expressed at significantly higher levels in breast cancer (BC) cell line than in normal breast cell line with co-localized with Dishevelled (DVL) in the cytoplasm of BC cell line. TMEM88 silencing in the ovarian cancer cell line CP70 resulted in significant upregulation of Wnt downstream genes (c-Myc, cyclin-D1) and other Wnt target genes including JUN, PTIX2, CTNNB1 (β-catenin), further supporting that TMEM88 inhibits canonical Wnt signaling pathway. Wnt signaling pathway has been known to play important roles in many diseases, especially in cancer. For instance, hepatocellular carcinoma (HCC) has become one of the most common tumors harboring mutations in the Wnt signaling pathway. As the inhibitor of Wnt signaling, TMEM88 has been considered to act as an oncogene or a tumor suppressor. Up-regulated TMEM88 or gene therapy approaches could be an effective therapeutic approach against tumor as TMEM88 inhibits Wnt signaling through direct interaction with DVL. Here, we review the current knowledge on the functional role and potential clinical application of TMEM88 in the control of various cancers. HighlightsWnt signaling displays an important role in several pathogenesis of cancer.Wnt signaling pathway is activated during cancer development.TMEM88 has an impact on cancer by inhibiting canonical Wnt signaling.We discuss the importance and new applications of TMEM88 in cancer therapy. K E Y W O R D Sβ-catenin, cancer, cancer therapy, TMEM88, Wnt signalling pathway Abbreviations: 1,25(OH)2D3, 1,25-Dihydroxyvitamin D3; AKT/mTOR, protein kinase B/the mammalian target of rapamycin; ATF2, Activating transcription factor 2; BC, breast cancer; CBE, clinical breast exam; CIZ1b, b-variant form of CIZ1; CK1, casein kinase 1; CRD, cystein-rich domain; CTNNB1, catenin β1; Dnmt3a, DNA (cytosine-5)-methyltransferase 3A; DVL, dishevelled; EMT, epithelial-mesenchymal transition; FAK, focal adhesion kinase; FZD, frizzled; GSK3β, glycogen synthase kinase 3β; HCC, hepatocellular carcinoma; HSCs, hematopoietic stem cells; IDCs, invasive ductal carcinomas; LC, lung cancer; LRP5, low density lipoprotein receptor-related protein-5; METTL13, methyltransferase like 13; MMP-7, matrix metalloproteinase-7; MRI, magnetic resonance imaging; NSCLC, nonsmall cell lung cancer; OC, ovarian cancer; P38, protein 38; PFS, progression-free survival; TCF/LEF, T cell factor/lymphoid enhancer factor; TCGA, the cancer genome atlas; TMEM88, transmembrane protein 88; TNBC, triple-negative breast cancer; VWV, Val-Trp-Val; Zo-1, tight junction protein 1.Yun-xuan Ge, Chang-hui Wang, and Fu-yong Hu have contribute equally to this work.

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Section: Potential Clinical Application Of Tmem88 In Cancermentioning

confidence: 99%

New advances of TMEM88 in cancer initiation and progression, with special emphasis on Wnt signaling pathway

Wang

et al. 2017

Journal Cellular Physiology

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“…A study indicated that METTL13 inhibits apoptosis of lung, breast and liver cancer cells and miR-16 can repress the expression of METTL13 by binding to its 3′-untranslated region [ 8 ]. In 2016, researchers detected high expression levels of METTL13 in the plasma of patients with breast, ovarian and lung cancer [ 9 ], following which it was identified as a recurrence predictor for breast cancer [ 10 ]. As a methyltransferase protein, it can specifically methylate the Lys55 of eEF1A, resulting in the increase of its translational output and tumorigenesis of lung and pancreatic cancer [ 11 , 12 ].…”

Section: Introductionmentioning

confidence: 99%

“…Protein methyltransferase like 13 (METTL13), also called FEAT, is coded by gene METTL13, which is located at chromosome 1q24.3. Purified from rat livers in 2011 by a Japanese researcher, METTL13 was found to be abnormally overexpressed in several human cancers including lung cancer and to drive tumorigenesis in transgenic mice [7][8][9][10]. A study indicated that METTL13 inhibits apoptosis of lung, breast and liver cancer cells and miR-16 can repress the expression of METTL13 by binding to its 3′-untranslated region [8].…”

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confidence: 99%

METTL13 inhibits progression of clear cell renal cell carcinoma with repression on PI3K/AKT/mTOR/HIF-1α pathway and c-Myc expression

et al. 2021

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Background Clear cell renal cell carcinoma (ccRCC) is the most common and aggressive type of renal malignancy. Methyltransferase like 13 (METTL13) functions as an oncogene in most of human cancers, but its function and mechanism in ccRCC remains unreported. Methods qRT-PCR, western blotting and immunohistochemistry were used to detect METTL13’s expression in tissues. The effects of METTL13 on ccRCC cells’ growth and metastasis were determined by both functional experiments and animal experiments. Weighted gene co-expression network analysis (WGCNA) was performed to annotate METTL13’s functions and co-immunoprecipitation (co-IP) was used to determine the interaction between METTL13 and c-Myc. Results METTL13 was underexpressed in ccRCC tissues compared to normal kidney tissues and its low expression predicted poor prognosis for ccRCC patients. The in vitro studies showed that knockdown and overexpression of METTL13 respectively led to increase and decrease in ccRCC cells’ proliferation, viability, migratory ability and invasiveness as well as epithelial-mesenchymal transition (EMT). The in vivo experiment demonstrated the inhibitory effect that METTL13 had on ccRCC cells’ growth and metastasis. Bioinformatic analyses showed various biological functions and pathways METTL13 was involved in. In ccRCC cells, we observed that METTL13 could negatively regulate PI3K/AKT/mTOR/HIF-1α pathway and that it combined to c-Myc and inhibited c-Myc protein expression. Conclusions In general, our finding suggests that high expression of METTL13 is associated with favorable prognosis of ccRCC patients. Meanwhile, METTL13 can inhibit growth and metastasis of ccRCC cells with participation in multiple potential molecular mechanisms. Therefore, we suggest METTL13 can be a new diagnostic and therapeutic target for ccRCC in the future.

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“…After that, a study indicated that post-transcriptionally regulated by miR-16, it inhibits apoptosis of lung, breast and liver cancer cells [8]. In 2016, researchers detected high expression levels of METTL13 in the blood plasma of patients with breast, ovarian and lung cancer [9], following which it was identi ed as a recurrence predictor for breast cancer [10]. As a methyltransferase protein, it can speci cally di-methylate the Lys55 of eEF1A, resulting in the increase of its translational output and tumorigenesis of lung and pancreatic cancer [11,12].…”

Section: Introductionmentioning

confidence: 99%

METTL13 Inhibits Progression of Clear Cell Renal Cell Carcinoma with Repression on PI3K/AKT/mTOR/HIF-1α Pathway and c-Myc Expression

Liu

Sun

Piao

et al. 2021

Preprint

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Background: Clear cell renal cell carcinoma (ccRCC) is the most common and aggressive type of renal malignancy. Methyltransferase like 13 (METTL13) functions as an oncogene in most of human cancers, but its function and mechanism in ccRCC remain unreported. Methods: qRT-PCR, western blot and immunohistochemistry were used to detect METTL13’s expressions in tissues. The effects of METTL13 on ccRCC cells’ growth and metastasis were determined by both functional experiments and animal experiments. Weighted gene co-expression network analysis (WGCNA) was performed to annotate METTL13’s functions and co-immunoprecipitation (co-IP) was used to determine the interaction between two proteins. Results: METTL13 was lowly expressed in ccRCC tissues compared to normal kidney tissues and its low expression predicted poor prognosis for ccRCC patients. In vitro study indicated METTL13’s inhibition on ccRCC cells’ proliferation, viability, migratory ability and invasiveness as well as epithelial-mesenchymal transition (EMT). Bioinformatic analyses showed various biological functions and pathways METTL13 was involved in. In ccRCC cells, we observed that METTL13 could negatively regulate PI3K/AKT/mTOR/HIF-1α pathway and that it combined to c-Myc and inhibited c-Myc expression. In vivo experiment confirmed that METTL13 inhibited ccRCC cell growth and metastasis. Conclusions: In general, our finding suggests that associated with favorable prognosis of ccRCC patients, METTL13 can inhibit growth and metastasis of ccRCC cells with multiple potential molecular mechanisms. Therefore, it’s likely for METTL13 to serve as a new diagnostic and therapeutic target for ccRCC in the future.

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FEAT expression correlates with tumor size, PR status, HER2 expression, Ki67 index, and molecular subtype and predicts recurrence in breast cancer

Cited by 6 publications

References 22 publications

New advances of TMEM88 in cancer initiation and progression, with special emphasis on Wnt signaling pathway

New advances of TMEM88 in cancer initiation and progression, with special emphasis on Wnt signaling pathway

METTL13 inhibits progression of clear cell renal cell carcinoma with repression on PI3K/AKT/mTOR/HIF-1α pathway and c-Myc expression

METTL13 Inhibits Progression of Clear Cell Renal Cell Carcinoma with Repression on PI3K/AKT/mTOR/HIF-1α Pathway and c-Myc Expression

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