Evidence map›Paper›PMID 34328193›Full record

ArticleMolecular medicine reports2021

Knockdown of circ‑PVT1 inhibits the progression of lung adenocarcinoma and enhances the sensitivity to cisplatin via the miR‑429/FOXK1 signaling axis.

Limin Cao, Xuefeng Zhou, Xi Ding, Dongyun Gao

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
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  7. The Emerging Roles of CircPVT1 in Cancer Progression.Current pharmaceutical biotechnology · 2025
    Review
  8. Article
  9. Review
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  11. Article
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  16. lncRNA PVT1: a novel oncogene in multiple cancers.Cellular & molecular biology letters · 2022
    Review
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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

4 authors at 2 institutions in 1 country.

Limin CaoDepartment of Respiratory Medicine, The Second People's Hospital of Lianyungang, Lianyungang, Jiangsu 222023, P.R. China.
Xuefeng ZhouDepartment of Oncology, The Affiliated Hospital of Nantong University, Dongtai, Jiangsu 224200, P.R. China.
Xi DingDepartment of Pharmacy, The Affiliated Hospital of Nantong University, Dongtai, Jiangsu 224200, P.R. China.
Dongyun GaoDepartment of Oncology, The Affiliated Hospital of Nantong University, Dongtai, Jiangsu 224200, P.R. China.
Nantong University · CNThe First People’s Hospital of Lianyungang · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is one of the most prevalent cancers in China, and its incidence and morbidity remain high due to various independent factors. Lung adenocarcinoma (ADC) is the most common type of non‑small cell lung carcinoma. Circular RNA plasmacytoma variant translocation 1 (circ‑PVT1) plays an oncogenic role in various types of cancer, but the specific role of circ‑PVT1 in lung ADC has not yet been reported. In the present study, circ‑PVT1 was knocked down in A549 cells and the cell viability, proliferation, migration and invasion were measured via MTT, colony formation, wound healing and Transwell assays, respectively. Then, the cell viability of A549 cells with circ‑PVT1‑knockdown or ‑overexpression was detected after exposure to cisplatin (DDP). After confirming the associations among circ‑PVT1, microRNA (miR)‑429 and forkhead box k1 (FOXK1) using various tools and assays, the cellular functions of A549 cells treated with combined short hairpin (sh)RNA‑circ‑PVT1 and miR‑429 inhibitor/pcDNA3.1‑FOXK1 were tested again. The expression of circ‑PVT1 was found to be increased in lung ADC cells, and shRNA‑circ‑PVT1 led to decreased cell viability, proliferation, migration and invasion. The expression of circ‑PVT1 was higher in A549/DDP cells than that in A549 cells, and the activity of caspase‑3 was also activated by DDP in A549/DDP cells transfected with shRNA‑circ‑PVT1, whereas it was inactivated by DDP in A549 cells transfected with circ‑PVT1 overexpression plasmid. Furthermore, the decreased cell viability, proliferation, invasion and migration induced by shRNA‑circ‑PVT1 could be abated by transfection with miR‑429 inhibitor and pcDNA3.1‑FOXK1. In conclusion, interference of circ‑PVT1 inhibits the progression of lung ADC and enhances its sensitivity to DDP via miR‑429/FOXK1, which may provide a theoretical basis for the use of novel targets in the treatment of lung ADC.

Indexed as

A549 CellsAdenocarcinoma of LungAntineoplastic AgentsApoptosisCell MovementCell ProliferationCisplatinDrug Resistance, NeoplasmForkhead Transcription FactorsGene Knockdown TechniquesHumansLung NeoplasmsMicroRNAsRNA, CircularSignal TransductionAntineoplastic AgentsCisplatinForkhead Transcription FactorsFOXK1 protein, humanMicroRNAsMIRN429 microRNA, humanRNA, CircularcircRNA plasmacytoma variant translocation 1cisplatinforkhead box k1lung adenocarcinomamicroRNA‑429

Identifiers

PMID34328193
PMCPMC8365593
OpenAlexW3183521097

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.