Evidence map›Paper›PMID 35301287›Full record

ArticleCell death discovery2022

Claudin1 decrease induced by 1,25-dihydroxy-vitamin D3 potentiates gefitinib resistance therapy through inhibiting AKT activation-mediated cancer stem-like properties in NSCLC cells.

Zhirong Jia, Kaiwei Wang, Yalei Duan, Kaiyong Hu, Yameng Zhang, Meisa Wang, Kang Xiao, Shuo Liu, Zhenzhen Pan, Xuansheng Ding

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. 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

10 authors at 1 institution in 1 country.

Zhirong Jia *School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, 211198, Nanjing, China. rongyunshan@126.com.ORCID http://orcid.org/0000-0002-7381-5150
Kaiwei Wang *School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, 211198, Nanjing, China.
Yalei Duan *School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, 211198, Nanjing, China.
Kaiyong HuR&D Department, Hubei Monyan Pharmaceutical Co., Ltd, 448124, Jingmen, China.
Yameng ZhangSchool of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, 211198, Nanjing, China.
Meisa WangSchool of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, 211198, Nanjing, China.
Kang XiaoSchool of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, 211198, Nanjing, China.
Shuo LiuSchool of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, 211198, Nanjing, China.
Zhenzhen PanSchool of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, 211198, Nanjing, China.
Xuansheng DingSchool of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, 211198, Nanjing, China. 1020030749@cpu.edu.cn.
China Pharmaceutical University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82003861
6 · The paper itself

Abstract

Claudins, the integral tight junction proteins that regulate paracellular permeability and cell polarity, are frequently dysregulated in cancer; however, their roles in regulating EGFR tyrosine kinase inhibitors (EGFR-TKIs) resistance in non-small cell lung cancer (NSCLC) are unknown. To this end, we performed GEO dataset analysis and identified that claudin1 was a critical regulator of EGFR-TKI resistance in NSCLC cells. We also found that claudin1, which was highly induced by continuous gefitinib treatment, was significantly upregulated in EGFR-TKI-resistant NSCLC cells. By knocking down claudin1 in cell lines and xenograft models, we established that gefitinib resistance was decreased. Moreover, claudin1 knockdown suppressed the expression levels of pluripotency markers (Oct4, Nanog, Sox2, CD133, and ALDH1A1). Claudin1 loss inhibited phosphorylated AKT (p-AKT) expression and reduced cancer cell stemness by suppressing AKT activation. Furthermore, SKL2001, a β-catenin agonist, upregulated the expression levels of claudin1, p-AKT, and pluripotency markers, and 1,25-dihydroxy-vitamin D3 (1,25(OH)

Identifiers

PMID35301287
PMCPMC8931006
OpenAlexW4220948830

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.