Evidence map›Paper›PMID 33015042›Full record

ArticleFrontiers in cell and developmental biology2020

Regulation of MicroRNA-497-Targeting AKT2 Influences Tumor Growth and Chemoresistance to Cisplatin in Lung Cancer.

Lin Wang, Xiang-Bo Ji, Li-Hong Wang, Jian-Ge Qiu, Feng-Mei Zhou, Wen-Jing Liu, Di-di Wan, Marie Chai-Mi Lin, Ling-Zhi Liu, Jian-Ying Zhang and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 19 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 2 countries.

Lin WangThe First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Xiang-Bo JiBGI College & Henan Institute of Medical and Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, China.
Li-Hong WangBGI College & Henan Institute of Medical and Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, China.
Jian-Ge QiuThe First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Feng-Mei ZhouThe First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Wen-Jing LiuDepartment of Oncology, The Affiliated Cancer Hospital of Zhengzhou University (Henan Cancer Hospital), Zhengzhou, China.
Di-di WanBGI College & Henan Institute of Medical and Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, China.
Marie Chai-Mi LinThe First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Ling-Zhi LiuDepartment of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA, United States.
Jian-Ying ZhangBGI College & Henan Institute of Medical and Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, China.
Bing-Hua JiangThe First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Zhengzhou University · CNFirst Affiliated Hospital of Zhengzhou University · CNThomas Jefferson University · US

Funding

Chromium in carcinogenesis and angiogenesisR01ES027901 · NIEHS · UNIVERSITY OF IOWA · PI HE, JUN · 2018 to 2022
$1.6M
NIEHS NIH HHS R01 ES027901
6 · The paper itself

Abstract

backgroundMicroRNA-497 (miR-497) has been implicated in several cancers. Increasing studies demonstrate the role of AKT2 in cancers as an oncogene which is closely associated with tumor aggressiveness by enhancing cancer cell survival, migration and invasion However, miR-497/AKT2 axis in non-small cell lung cancer (NSCLC) remains unclear.

methodsQuantitative real-time PCR (qRT-PCR) was used to quantify the expression of miR-497 and its target gene. The function of miR-497 in lung cancer was investigated through

resultsIn this study, we found that miR-497 was significantly downregulated in tumor tissues and blood samples of lung cancer patients. To understand the potential mechanism of miR-497 in inhibiting tumor growth, we showed that miR-497 blocked the activation of AKT2 and regulated cell proliferation, cell migration, colony formation and increases chemosensitivity of H1299 cells to cisplatin by inhibiting AKT2. MiR-497 also inhibited tumor growth and suppressed expression of AKT2 at the protein and mRNA levels in mouse xenograft tumors.

conclusionTaken together, our findings indicated that miR-497 suppresses the tumor growth by targeting AKT2, and the miR-497/AKT2 axis is a potential therapeutic target for NSCLC intervention.

Indexed as

AKT2chemoresistancemiR-497NSCLCtumor growth

Identifiers

PMID33015042
PMCPMC7505950
OpenAlexW3084194434

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.