CD36 promotes the epithelial–mesenchymal transition and metastasis in cervical cancer by interacting with TGF-β

Deng, Min; Cai, Xiaodong; Long, Ling; Xie, Linying; Ma, Hongmei; Zhou, Yumin; Liu, Shuguang; Zeng, Chao

doi:10.1186/s12967-019-2098-6

Cited by 66 publications

(75 citation statements)

References 27 publications

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“…In the tumor microenvironment, cervical cancer-associated fibroblasts enhance the ability of cervical cancer cells to invade by secreting TGF-β ( Nagura et al, 2015 ). Deng et al (2019) revealed that CD36 binds to TGF-β to promote EMT, which leads to the migration and invasion of cervical cancer. Twist also regulates EMT via the TGF beta signaling pathway and promotes the migration of cervical cancer cells ( Fan et al, 2015 ).…”

Section: Discussionmentioning

confidence: 99%

Six-lncRNA Immune Prognostic Signature for Cervical Cancer

Chen

Huang

et al. 2020

Front. Genet.

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Background This study searched for immune-related long noncoding RNAs (lncRNAs) to predict the prognosis of patients with cervical cancer. Method We obtained immunologically relevant lncRNA expression profiles and clinical follow-up data from cervical cancer patients from The Cancer Genome Atlas database and the Molecular Signatures Database. Cervical cancer patients were randomly divided into a training group, testing group and combined group. The immune prognostic signature was constructed by Least Absolute Shrinkage and Selection Operator Cox regression, prognosis was analyzed by Kaplan–Meier curves between different groups, and the accuracy of the prognostic model was assessed by receiver operating characteristic-area under the curve (ROC-AUC) analysis. Results A six-lncRNA immune prognostic signature (LIPS) was constructed to predict the prognosis of cervical cancer. The six lncRNAs are as follows: AC009065.8, LINC01871, MIR210HG, GEMIN7-AS1, GAS5-AS1, and DLEU1. A ROC-AUC analysis indicated that the model could predict the prognosis of cervical cancer patients in different subgroups. A Kaplan–Meier analysis showed that patients with high risk scores had a poor prognosis; these results were equally meaningful in the subgroup analyses. Risk scores differed depending on the clinical pathology and tumor grade and were independent risk factors for cervical cancer prognosis. Gene set enrichment analysis revealed an association between the LIPS and the immune response, Wnt signaling pathway, and TGF beta signaling pathway. Conclusion Our study shows that the six-LIPS can predict the prognosis of cervical cancer and contribute to decisions regarding the immunotherapeutic strategy.

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Section: Discussionmentioning

confidence: 99%

Six-lncRNA Immune Prognostic Signature for Cervical Cancer

Chen

Huang

et al. 2020

Front. Genet.

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“…CD36 contributes to the progression and metastatic potential of cancer by several mechanisms, such as activation of cancer stem cells, epithelial-to-mesenchymal transition, and chemoresistance [35,36].…”

Section: Cd36 Promotes Tumor Metastasis In Pancreatic Cancermentioning

confidence: 99%

“…Taking into consideration that these two markers were separately described in different studies [35,53,71,79] as conferring an invasive phenotype, silencing both their expression could affect the physiopathology of the disease.…”

Section: Why Examine Concomitant Expression Of Cd36 and Cd97s? (Why Bmentioning

confidence: 99%

CD36 and CD97 in Pancreatic Cancer versus Other Malignancies

Tănase

Gheorghișan-Gălățeanu

Popescu

et al. 2020

IJMS

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Starting from the recent identification of CD36 and CD97 as a novel marker combination of fibroblast quiescence in lung during fibrosis, we aimed to survey the literature in search for facts about the separate (or concomitant) expression of clusters of differentiation CD36 and CD97 in either tumor- or pancreatic-cancer-associated cells. Here, we provide an account of the current knowledge on the diversity of the cellular functions of CD36 and CD97 and explore their potential (common) contributions to key cellular events in oncogenesis or metastasis development. Emphasis is placed on quiescence as an underexplored mechanism and/or potential target in therapy. Furthermore, we discuss intricate signaling mechanisms and networks involving CD36 and CD97 that may regulate different subpopulations of tumor-associated cells, such as cancer-associated fibroblasts, adipocyte-associated fibroblasts, tumor-associated macrophages, or neutrophils, during aggressive pancreatic cancer. The coexistence of quiescence and activated states in cancer-associated cell subtypes during pancreatic cancer should be better documented, in different histological forms. Remodeling of the local microenvironment may also change the balance between growth and dormant state. Taking advantage of the reported data in different other tissue types, we explore the possibility to induce quiescence (similar to that observed in normal cells), as a therapeutic option to delay the currently observed clinical outcome.

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“…The majority of early cancer is detected via refined detection technology, and the mortality of CC has apparently declined, and the prognosis rate has been elevated 6 . However, patients with advanced CC still have unpleasant endings because of the high onset of metastasis, which is a main element affecting the prognosis of patients 7 . Cancer stem cells strengthen tumor‐initiating and self‐renewing abilities 8 .…”

Section: Introductionmentioning

confidence: 99%

“…6 However, patients with advanced CC still have unpleasant endings because of the high onset of metastasis, which is a main element affecting the prognosis of patients. 7 Cancer stem cells strengthen tumor-initiating and self-renewing abilities. 8 At present, no therapies are able to eliminate cancer stem cells, and their presence leads to poor prognosis in CC.…”

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confidence: 99%

Elevated microRNA‐130b‐5p or silenced ELK1 inhibits self‐renewal ability, proliferation, migration, and invasion abilities, and promotes apoptosis of cervical cancer stem cells

Huang

Luo

2020

IUBMB Life

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Cervical cancer (CC) is the most familiar gynecological malignancy. With the poor prognosis of CC patients, this study explored the effect of microRNA (miR)‐130b‐5p targeting ELK1 expression on self‐renewal ability and stemness of CC stem cells. The tissues of patients with CC or cervical benign lesions were collected. MiR‐130b‐5p and ELK1 expression was detected by reverse transcription quantitative polymerase chain reaction and western blot analysis. Human CC cell line Hela was cultured and the induced CC stem cells were introduced with miR‐130b‐5p mimic or silenced ELK1 to figure their roles in self‐renewal ability, stemness, colony formation, proliferation, migration, invasion abilities, and apoptosis of CC stem cells. Tumor growth was detected in nude mice in vivo. The targeting relationship between miR‐130b‐5p and ELK1 was analyzed using bioinformatic prediction and dual luciferase reporter gene assay. Decreased miR‐130b‐5p and elevated ELK1 existed in CC tissues of patients. Up‐regulated miR‐130b‐5p decreased ELK1 expression in CC stem cells. Elevated miR‐130b‐5p or silenced ELK1 inhibited self‐renewal ability and stemness, colony formation, proliferation, migration and invasion abilities, promoted apoptosis of CC stem cells, as well as decreased the weight and volume of tumor in nude mice. ELK1 was found to be targeted by miR‐130b‐5p. Overexpression ELK1 effectively reversed the cellular phenotypic changes and tumor formation in vivo caused by up‐regulation of miR‐130b‐5p. We conclude that up‐regulated miR‐130b‐5p or silenced ELK1 inhibits CC stem cell growth.

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CD36 promotes the epithelial–mesenchymal transition and metastasis in cervical cancer by interacting with TGF-β

Cited by 66 publications

References 27 publications

Six-lncRNA Immune Prognostic Signature for Cervical Cancer

Six-lncRNA Immune Prognostic Signature for Cervical Cancer

CD36 and CD97 in Pancreatic Cancer versus Other Malignancies

Elevated microRNA‐130b‐5p or silenced ELK1 inhibits self‐renewal ability, proliferation, migration, and invasion abilities, and promotes apoptosis of cervical cancer stem cells

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