Evidence map›Paper›PMID 32648226›Full record

ArticleJournal of cancer research and clinical oncology2020

A novel metastatic promoter CEMIP and its downstream molecular targets and signaling pathway of cellular migration and invasion in SCLC cells based on proteome analysis.

Li Li, Yingxing Pan, Xiaoxiang Mo, Tongtong Wei, Jinjing Song, Min Luo, Guolin Huang, Cuifang Teng, Kai Liang, Naiquan Mao and 1 more

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. 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

11 authors at 2 institutions in 1 country.

Li LiDepartment of Pharmacology, School of Pharmacy, Guangxi Medical University, Nanning, 530021, Guangxi, People's Republic of China.
Yingxing PanDepartment of Pharmacology, School of Pharmacy, Guangxi Medical University, Nanning, 530021, Guangxi, People's Republic of China.
Xiaoxiang MoDepartment of Pharmacology, School of Pharmacy, Guangxi Medical University, Nanning, 530021, Guangxi, People's Republic of China.
Tongtong WeiDepartment of Pharmacology, School of Pharmacy, Guangxi Medical University, Nanning, 530021, Guangxi, People's Republic of China.
Jinjing SongDepartment of Pharmacology, School of Pharmacy, Guangxi Medical University, Nanning, 530021, Guangxi, People's Republic of China.
Min LuoDepartment of Pharmacy, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning, 530001, Guangxi, People's Republic of China.
Guolin HuangDepartment of Pharmacology, School of Pharmacy, Guangxi Medical University, Nanning, 530021, Guangxi, People's Republic of China.
Cuifang TengDepartment of Pharmacology, School of Pharmacy, Guangxi Medical University, Nanning, 530021, Guangxi, People's Republic of China.
Kai LiangDepartment of Thoracic Tumor Surgery, The Affiliated Cancer Hospital of Guangxi Medical University, Nanning, 530021, Guangxi, People's Republic of China.
Naiquan MaoDepartment of Thoracic Tumor Surgery, The Affiliated Cancer Hospital of Guangxi Medical University, Nanning, 530021, Guangxi, People's Republic of China.
Jie YangDepartment of Pharmacology, School of Pharmacy, Guangxi Medical University, Nanning, 530021, Guangxi, People's Republic of China. jieyang2016@gxmu.edu.cn.ORCID http://orcid.org/0000-0002-8393-3580
Guangxi Medical University · CNGuangxi University · CN

Funding

Guangxi First-class Discipline Project for Pharmaceutical Sciences GXFCDP-PS-2018Guangxi Natural Science Foundation Program 2018GXNSFAA050053Innovation Project of Guangxi Graduate Education YCBZ2020054Innovative Research Group Project of the National Natural Science Foundation of China 81860649
6 · The paper itself

Abstract

purposeMetastasis is an unavoidable event happened among almost all small cell lung cancer (SCLC) patients. However, the molecular driven factors have not been elucidated. Recently, a novel hydrolase called cell migration inducing hyaluronidase (CEMIP) triggered both migration and invasion in many tumors but not SCLC. Therefore, in this study, we verified that CEMIP promoted migration and invasion in SCLC and applied proteomics analysis to screen out potential target profiles and the signaling pathway related to CEMIP regulation.

methodImmunofluorescence was conducted to exam the expression of CEMIP on SCLC and paired adjacent normal tissues among enrollment. RT-qPCR and Western blot (WB) assays were conducted to valuate cellular protein and mRNA expression of CEMIP and EMT markers. Lentivirus-CEMIP-shRNAs and CEMIP plasmid were used for expression manipulating. Changes of cellular migration and invasion were tested through transwell assays. Tandem Mass Tag (TMT) peptide labeling coupled with LC-MS/MS was used for quantifying proteins affected by reducing expression of CEMIP on H446 cells.

resultsThe expression of CEMIP showed 1.64 ± 0.16-fold higher in SCLC tissues than their normal counterpart. Decreasing the expression of CEMIP on SCLC cells H446 regressed both cellular migration and invasion ability, whereas the promoting cellular migration and invasion was investigated through over-expressing CEMIP on H1688. Proteomic and bioinformatics analysis revealed that total 215 differentially expressed proteins (DEPs) that either their increasing or decreasing relative expression met threshold of 1.2-fold changes with p value ≤ 0.05. The dramatic up-regulated DEPs included an unidentified peptide sequence (encoded by cDNA FLJ52096) SPICE1 and CRYAB, while the expression of S100A6 was largely down-regulated. DEPs mainly enriched on caveolae of cellular component, calcium ion binding of biological process and epithelial cell migration of molecular function. KEGG enrichment indicated that DEPs mainly exerted their function on TGF-β, GABAergic synapse and MAPK signaling pathway.

conclusionIt is the first report illustrating that CEMIP might be one of the metastatic triggers in SCLC. And also, it provided possible molecular mechanism cue and potential downstream target on CEMIP-induced cellular migration and invasion on SCLC.

Indexed as

AgedCell Line, TumorCell MovementFemaleFluorescent Antibody TechniqueHumansHyaluronoglucosaminidaseLung NeoplasmsMaleMiddle AgedNeoplasm InvasivenessProteomeRetrospective StudiesSignal TransductionSmall Cell Lung CarcinomaCEMIP protein, humanHyaluronoglucosaminidaseProteomeCEMIPMetastasisProteome analysisSCLCSignaling pathway

Identifiers

PMID32648226
PMCPMC11804513
OpenAlexW3041851155

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.