Evidence map›Paper›PMID 35173830›Full record

ArticleAmerican journal of translational research2022

The molecular mechanism of kinesin family member 2A (KIF2A) underlying non-small cell lung cancer: the effect of its knockdown on malignant behaviors, stemness, chemosensitivity, and potential regulated signaling pathways.

Jiayan Chen, Junmiao Wen, Di Liu, Xinyan Xu, Min Fan, Zhen Zhang

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 45% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
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  4. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Jiayan ChenDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center Shanghai, China.
Junmiao WenDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center Shanghai, China.
Di LiuDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center Shanghai, China.
Xinyan XuDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center Shanghai, China.
Min FanDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center Shanghai, China.
Zhen ZhangDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center Shanghai, China.
Shanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kinesin family member 2A (KIF2A) represents an oncogene in several cancers, however, its involvement in non-small cell lung cancer (NSCLC) is limitedly investigated. Therefore, the present study aimed to explore potential molecular mechanism of KIF2A knockdown in repressing NSCLC malignant behaviors. The effect of KIF2A knockdown on cell proliferation, apoptosis, invasion, epithelial-mesenchymal transition (EMT) markers, stemness, chemosensitivity was detected after transfecting KIF2A short hairpin RNA (ShRNA) plasmids into A549 and NCI-H1975 cells. Moreover, KIF2A knockdown mediated signaling pathways were analyzed by RNA sequencing (RNA-seq), and then validated by western blot assay. Both KIF2A mRNA and protein expressions were increased in A549, NCI-H650, NCI-H358, NCI-H2106, NCI-H1299, NCI-H1650 and NCI-H1975 cells compared with BEAS-2B cells. KIF2A knockdown inhibited proliferation, invasion, EMT, stemness, but enhanced chemosensitivity to cisplatin and paclitaxel in both A549 and NCI-H1975 cells. Meanwhile, it only promoted apoptosis in NCI-H1975 cells but not in A549 cells. Moreover, after KIF2A knocking down, RNA-seq data indicated that 356 accordant differentially expressed genes (DEGs) in both A549 and NCI-H1975 cells, and these DEGs were enriched in PI3K-Akt, Wnt and Notch signaling pathways. Further western blot disclosed that KIF2A knockdown indeed inactivated PI3K-Akt, Wnt and Notch signaling pathways in both A549 and NCI-H1975 cells. In conclusion, KIF2A knockdown suppresses NSCLC cell malignant behaviors, EMT and stemness, but enhances chemosensitivity via inactivating PI3K-Akt, Wnt, and Notch signaling pathways, which proposes it as a potential therapeutic target for NSCLC treatment.

Indexed as

chemosensitivityKinesin family member 2Amalignant behaviorsnon-small cell lung cancerRNA-sequencing

Identifiers

PMID35173830
PMCPMC8829653
OpenAlexW4213392406

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.