Evidence map›Paper›PMID 34850004›Full record

ArticleJournal of biochemistry2022

CircRPPH1 promotes cell proliferation, migration and invasion of non-small cell lung cancer via the PI3K/AKT and JAK2/STAT3 signalling axes.

Jian-Wen Xiong, Si-Bei Song, Lin-Min Xiong, Chuan-Hui Duan, Qian Song, Dong-Liang Yu, Xiao-Qiang Zhang

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Journal of biochemistry, 2022. 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 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Article
  3. C-Fos-activated circRPPH1 contributes to glioma stemness.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Article
  4. Article
  5. Review
  6. Article
  7. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Jian-Wen XiongDepartment of Thoracic Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.
Si-Bei SongDepartment of Gastroenterology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.
Lin-Min XiongDepartment of Thoracic Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.
Chuan-Hui DuanDepartment of Thoracic Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.
Qian SongDepartment of Thoracic Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.
Dong-Liang YuDepartment of Thoracic Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.
Xiao-Qiang ZhangDepartment of Thoracic Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.
Nanchang University · CNSecond Affiliated Hospital of Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-small cell lung cancer (NSCLC) has markedly increased morbidity and mortality rates worldwide. Circular RNAs were shown to regulate NSCLC progression. But the underlying pathways of the circRPPH1-mediated regulation of NSCLC still need further exploration. We evaluated circRPPH1 levels in NSCLC tissues and cell lines via qRT-PCR. Moreover, using ectopic plasmid incorporation and siRNA assays, we analysed the circRPPH1-mediated regulation of cell proliferation (CP), cell migration (CM) and cell invasion (CI) in NSCLC cell lines (H1975 and A549 cells), using CCK-8, colony forming, scratch wound and transwell assays, respectively. CircRPPH1 levels were remarkably high in the NSCLC tissues and cell lines. The transfection experiments showed that circRPPH1 overexpression was able to promote CP, CM and CI of NSCLC cells, while CP, CM and CI were significantly restrained by the knockdown of circRPPH1. We also displayed that circRPPH1 knockdown suppressed the cell progression via inactivating the PI3K/AKT and JAK2/STAT3 signalling axes. Subsequently, in vivo experiment in nude mice was demonstrated that the inhibition of circRPPH1 could reduce the tumour growth of NSCLC. circRPPH1 may accelerate the growth and metastasis of NSCLC, in culture conditions and in animal models, by stimulating the PI3K/AKT and JAK2/STAT3 signalling axes, thus promoting the development of NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsAnimalsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansMiceMice, NudePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktcircRPPH1JAK2/STAT3NSCLCPI3K/AKT

Identifiers

PMID34850004
OpenAlexW3216921272

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.