Evidence map›Paper›PMID 26474873›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2016

Overexpression of Cathepsin L is associated with gefitinib resistance in non-small cell lung cancer.

F Cui, W Wang, D Wu, X He, J Wu, M Wang

Abstract read
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In one paragraph

Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2016. 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
2.1field-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

14 citing papers in PubMed, 18 citations in OpenAlex.

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  12. The Air Sac Primordium ofInternational journal of molecular sciences · 2018
    Review
  13. Article
  14. Yellow and green pigments fromOncology letters · 2018
    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

6 authors at 3 institutions in 1 country.

F CuiDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, People's Republic of China.
W WangDepartment of Thoracic Surgery, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, No. 107 Yanjiangxi Road, Guangzhou, 510120, People's Republic of China.
D WuDepartment of Thoracic Surgery, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, No. 107 Yanjiangxi Road, Guangzhou, 510120, People's Republic of China.
X HeDepartment of Thoracic Surgery, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, No. 107 Yanjiangxi Road, Guangzhou, 510120, People's Republic of China.
J WuPharmaceutical Department, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, No. 107 Yanjiangxi Road, Guangzhou, 510120, People's Republic of China. drwujy67@163.com.
M WangDepartment of Thoracic Surgery, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, No. 107 Yanjiangxi Road, Guangzhou, 510120, People's Republic of China. drwangxh@163.com.
Sun Yat-sen University · CNSun Yat-sen Memorial Hospital · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer, the most common malignancy, is still the leading cause of cancer-related death worldwide. Non-small-cell lung cancer (NSCLC) accounts for 80 % of all lung cancers. Recent studies showed Cathepsin L (CTSL) is overexpressed in various cancerous tissues; however, the association between CTSL expression and EGFR-TKI resistance remains unknown. In this study, we investigated the expression of CTSL in lung cancer specimens and matched normal tissues by quantitative real-time PCR and IHC. The functional role of CTSL in resistant PC-9/GR cell line was investigated by proliferation and apoptosis analysis compared with control PC-9 cells. Our results found that the level of CTSL expression was higher in NSCLC tissues compared with matched normal adjacent tissue samples, and CTSL was more highly expressed in PC-9/GR cells compared to PC-9 cells. Knocking-down of CTSL in PC-9/GR cells could decrease cell proliferation and potentiate apoptosis induced by gefitinib, suggesting CTSL may contribute to gefitinib resistance in NSCLC. CTSL might be explored as a candidate of therapeutic target for modulating EGFR-TKI sensitivity in NSCLC.

Indexed as

Antineoplastic AgentsApoptosisBiomarkers, TumorBlotting, WesternCarcinoma, Non-Small-Cell LungCathepsin LCell ProliferationDrug Resistance, NeoplasmGefitinibHumansImmunohistochemistryLung NeoplasmsQuinazolinesReal-Time Polymerase Chain ReactionAntineoplastic AgentsBiomarkers, TumorCathepsin LCTSL protein, humanGefitinibQuinazolinesApoptosisChemoresistanceCTSLEGFR-TKILung cancerNSCLCPC-9/GR cellsProliferation

Identifiers

PMID26474873
OpenAlexW1896721440

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.