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Oncology Reports
Article
License: CC BY NC ND
Data sources: UnpayWall
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PubMed Central
Article . 2021
Data sources: PubMed Central
Oncology Reports
Article . 2020 . Peer-reviewed
Data sources: Crossref
Oncology Reports
Article . 2021
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Erb‑B2 Receptor Tyrosine Kinase 2 is negatively regulated by the p53‑responsive microRNA‑3184‑5p in cervical cancer cells

Authors: Liu, Hongli; Li, Yuzhi; Zhang, Jing; Wu, Nan; Liu, Fei; Wang, Lihua; Zhang, Yuan; +4 Authors

Erb‑B2 Receptor Tyrosine Kinase 2 is negatively regulated by the p53‑responsive microRNA‑3184‑5p in cervical cancer cells

Abstract

The oncogenic role of Erb‑B2 Receptor Tyrosine Kinase 2 (ERBB2) has been identified in several types of cancer, but less is known on its function and mechanism of action in cervical cancer cells. The present study employed a multipronged approach to investigate the role of ERBB2 in cervical cancer. ERBB2 and microRNA (miR)‑3184‑5p expression was assessed in patient‑derived cervical cancer biopsy tissues, revealing that higher levels of ERBB2 and lower levels of miR‑3184‑5p were associated with clinicopathological indicators of cervical cancer progression. Furthermore, ERBB2 stimulated proliferation, migration and sphere‑formation of cervical cancer cells in vitro. This effect was mediated by enhanced phosphatidylinositol‑4,5‑bisphosphate 3‑kinase catalytic subunit α activity. Additionally, it was revealed that miR‑3184‑5p directly suppressed ERBB2 in cervical cancer cells. The p53 activator Mithramycin A stimulated p53 and miR‑3184‑5p expression, thereby lowering the levels of ERBB2 and attenuating proliferation, migration and sphere‑formation of cervical cancer cells. In conclusion, the findings of the present study suggested ERBB2 as an oncogenic protein that may promote invasiveness in cervical cancer cells. Treatment of cervical cancer cells with the p53 activator Mithramycin A restored the levels of the endogenous ERBB2 inhibitor miR‑3184‑5p and may represent a novel treatment strategy for cervical cancer.

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Keywords

Adult, Class I Phosphatidylinositol 3-Kinases, Biopsy, Uterine Cervical Neoplasms, Articles, Cervix Uteri, Plicamycin, Middle Aged, Hysterectomy, Erb-b2 Receptor Tyrosine Kinases, Gene Expression Regulation, Neoplastic, MicroRNAs, Cell Movement, Cell Line, Tumor, Humans, Female, Neoplasm Invasiveness, Tumor Suppressor Protein p53, Aged, Cell Proliferation

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    selected citations
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    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
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    popularity
    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
    Top 10%
    influence
    This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    Top 10%
    impulse
    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Top 10%
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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
34
Top 10%
Top 10%
Top 10%
Green
hybrid
Related to Research communities
Cancer Research