Evidence map›Paper›PMID 35280763›Full record

ArticleFrontiers in oncology2022

COL8A1 Promotes NSCLC Progression Through IFIT1/IFIT3-Mediated EGFR Activation.

Xiangyi Zan, Shuyan Li, Shixiong Wei, Liping Gao, Lanting Zhao, Xiaoxia Yan, Yan Zhao, Junnian Shi, Yuping Wang, Rong Liu and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. ZNF714 Supports Pro-Oncogenic Features in Lung Cancer Cells.International journal of molecular sciences · 2023
    Article
  12. Article
  13. Article
  14. Article
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

13 authors at 5 institutions in 2 countries.

Xiangyi ZanDepartment of Pneumology, The Second Hospital of Lanzhou University, Lanzhou, China.
Shuyan LiDepartment of Chemistry and Chemical Engineering, Lanzhou University, Lanzhou, China.
Shixiong WeiBiological Science, University of California, Davis, Davis, CA, United States.
Liping GaoDepartment of Pneumology, The Second Hospital of Lanzhou University, Lanzhou, China.
Lanting ZhaoDepartment of Pneumology, The Second Hospital of Lanzhou University, Lanzhou, China.
Xiaoxia YanDepartment of Pneumology, The Second Hospital of Lanzhou University, Lanzhou, China.
Yan ZhaoDepartment of Pneumology, The Second Hospital of Lanzhou University, Lanzhou, China.
Junnian ShiDepartment of Pneumology, The Second Hospital of Lanzhou University, Lanzhou, China.
Yuping WangDepartment of Gastroenterology, The First Hospital of Lanzhou University, Lanzhou, China.
Rong LiuDepartment of Gastroenterology, The First Hospital of Lanzhou University, Lanzhou, China.
Yuanyi ZhangClinical Medicine, University of South China, Hengyang, China.
Yixin WanDepartment of Pneumology, The Second Hospital of Lanzhou University, Lanzhou, China.
Yongning ZhouDepartment of Gastroenterology, The First Hospital of Lanzhou University, Lanzhou, China.
Lanzhou University Second Hospital · CNLanzhou University · CNFirst Hospital of Lanzhou University · CNUniversity of California, Davis · USUniversity of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of EGFR is a major risk factor for non-small cell lung cancer (NSCLC). Understanding the molecular events promoting EGFR activation can help us gain more insights into the progression of NSCLC. In this study, we demonstrate that collagen type VIII alpha 1 chain (COL8A1), an extracellular matrix component, was overexpressed in NSCLC. In NSCLC cells, knockdown of COL8A1 suppressed cell growth, cycle progression, and migration, and induced cell apoptosis. While COL8A1 overexpression promoted cell proliferation and inhibited cell apoptosis. In addition, we found that COL8A1 depletion reduced interferon response signaling and downregulated (IFIT1) and interferon-induced proteins with tetratricopeptide repeats 3 (IFIT3). Moreover, we indicated that COL8A1 could upregulate IFIT1 and IFIT3 mediated EGFR activation

Indexed as

COL8A1EGFRIFIT1IFIT3NSCLC

Identifiers

PMID35280763
PMCPMC8907630
OpenAlexW4213442765

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.