<i>EMP2</i> re-expression inhibits growth and enhances radiosensitivity in nasopharyngeal carcinoma

Tang, Ming; Liu, Ru-Yan; Zhou, Cong; Yuan, Manman; Wu, Dongming; Zhu, Yong‐Guan; Zhang, Peng; Lang, Jinyi

doi:10.1177/1010428317695972

Cited by 8 publications

(6 citation statements)

References 31 publications

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“…EMP3 is induced by TWIST1/2 and regulates epithelial-to-mesenchymal transition of gastric cancer cells [30]. In line with the role of EMP2 in nasopharyngeal cancer and melanoma [31,32], EMP2 overexpression inhibited cell proliferation, migration, and invasion and caused G1 cell cycle arrest, while downregulation of EMP2 by siRNA resulted in an enhanced cell migratory ability. We did not perform proliferation assay after EMP2 knockdown, since the downregulation of EMP2 by siRNA was transient and could be recovered after 3-4 days, while the observation time for the proliferation assay was 5-day long.…”

Section: Discussionmentioning

confidence: 69%

Epithelial Membrane Protein 2 Suppresses Non-Small Cell Lung Cancer Cell Growth by Inhibition of MAPK Pathway

Schröder

Nenkov

et al. 2021

IJMS

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Epithelial membrane proteins (EMP1-3) are involved in epithelial differentiation and carcinogenesis. Dysregulated expression of EMP2 was observed in various cancers, but its role in human lung cancer is not yet clarified. In this study, we analyzed the expression of EMP1-3 and investigated the biological function of EMP2 in non-small cell lung cancer (NSCLC). The results showed that lower expression of EMP1 was significantly correlated with tumor size in primary lung tumors (p = 0.004). Overexpression of EMP2 suppressed tumor cell growth, migration, and invasion, resulting in a G1 cell cycle arrest, with knockdown of EMP2 leading to enhanced cell migration, related to MAPK pathway alterations and disruption of cell cycle regulatory genes. Exosomes isolated from transfected cells were taken up by tumor cells, carrying EMP2-downregulated microRNAs (miRNAs) which participated in regulation of the tumor microenvironment. Our data suggest that decreased EMP1 expression is significantly related to increased tumor size in NSCLC. EMP2 suppresses NSCLC cell growth mainly by inhibiting the MAPK pathway. EMP2 might further affect the tumor microenvironment by regulating tumor microenvironment-associated miRNAs.

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Section: Discussionmentioning

confidence: 69%

Epithelial Membrane Protein 2 Suppresses Non-Small Cell Lung Cancer Cell Growth by Inhibition of MAPK Pathway

Schröder

Nenkov

et al. 2021

IJMS

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“…EMP2 re-expression significantly suppressed cell growth and promoted radiosensitivity and cell apoptosis in CNE-2 cells. Thus, EMP2 is down-regulated and serves as a potential tumor suppressor gene in NPC cells [ 44 ]. In parallel, as shown in Figure 7A-7B , q-RT-PCR showed that miR-101-3p down-regulates EMP2 in NPC tissues; however, there is no relationship between miR-101-3p and EMP2 in normal nasopharyngeal epithelial tissues.…”

Section: Resultsmentioning

confidence: 99%

Long non-coding RNA NEAT1 regulates epithelial membrane protein 2 expression to repress nasopharyngeal carcinoma migration and irradiation-resistance through miR-101-3p as a competing endogenous RNA mechanism

Wang

Chen

et al. 2017

Oncotarget

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The altered expression of long non-coding RNAs (lncRNAs) is often related to carcinogenesis, metastasis and resistance to radiation or chemotherapy. In the current study, cDNA microarray analysis found that NEAT1 expression was reduced in nasopharyngeal carcinoma (NPC) patients and that it regulated NPC progression. However, the detailed mechanisms of NEAT1 in NPC were unclear. NEAT1 repressed NPC cell growth, invasion and radiation resistance in vitro and tumor metastasis in vivo. In addition, the results of an approach integrating bioinformatics, luciferase reporter assays and RNA immunoprecipitation indicated that NEAT1 antagonized miR-101-3p through a competing endogenous RNA (ceRNA) mechanism and that the interaction between NEAT1 and EMP2 was miR-101-3p dependent. Our results showed a novel connection of NEAT1, miR-101-3p and EMP2 in NPC migration and radiation resistance.

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“…In nasopharyngeal carcinoma, EMP2 can exist as a tumor suppressor. EMP2 can induce apoptosis in the CNE-2 nasopharyngeal carcinoma cell line and expose cells to radiotherapy [ 119 ]. The lncRNA nuclear enriched abundant transcript 1 (NEAT1) can affect EMP2 expression via miR-101-3p and slow the progression of nasopharyngeal carcinoma [ 120 ].…”

Section: Biological Functions Of the Pmp22 Protein Familymentioning

confidence: 99%

Unraveling the structures, functions and mechanisms of epithelial membrane protein family in human cancers

et al. 2022

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Peripheral myelin protein 22 (PMP22) and epithelial membrane proteins (EMP-1, -2, and -3) belong to a small hydrophobic membrane protein subfamily, with four transmembrane structures. PMP22 and EMPs are widely expressed in various tissues and play important roles in cell growth, differentiation, programmed cell death, and metastasis. PMP22 presents its highest expression in the peripheral nerve and participates in normal physiological and pathological processes of the peripheral nervous system. The progress of molecular genetics has shown that the genetic changes of the PMP22 gene, including duplication, deletion, and point mutation, are behind various hereditary peripheral neuropathies. EMPs have different expression patterns in diverse tissues and are closely related to the risk of malignant tumor progression. In this review, we focus on the four members in this protein family which are related to disease pathogenesis and discuss gene mutations and post-translational modification of them. Further research into the interactions between structural alterations and function of PMP22 and EMPs will help understand their normal physiological function and role in diseases and might contribute to developing novel therapeutic tools.

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EMP2 re-expression inhibits growth and enhances radiosensitivity in nasopharyngeal carcinoma

Cited by 8 publications

References 31 publications

Epithelial Membrane Protein 2 Suppresses Non-Small Cell Lung Cancer Cell Growth by Inhibition of MAPK Pathway

Epithelial Membrane Protein 2 Suppresses Non-Small Cell Lung Cancer Cell Growth by Inhibition of MAPK Pathway

Long non-coding RNA NEAT1 regulates epithelial membrane protein 2 expression to repress nasopharyngeal carcinoma migration and irradiation-resistance through miR-101-3p as a competing endogenous RNA mechanism

Unraveling the structures, functions and mechanisms of epithelial membrane protein family in human cancers

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