Evidence map›Paper›PMID 26992205›Full record

ArticleOncotarget2016

Increased chemoresistance via Snail-Raf kinase inhibitor protein signaling in colorectal cancer in response to a nicotine derivative.

Tsai-Yu Lee, Chia-Lin Liu, Yun-Ching Chang, Shin Nieh, Yaoh-Shiang Lin, Shu-Wen Jao, Su-Feng Chen, Tsung-Yun Liu

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  5. Review
  6. Article
  7. Multi-Omics Analysis of the Effects of Smoking on Human Tumors.Frontiers in molecular biosciences · 2021
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  12. 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

8 authors at 5 institutions in 1 country.

Tsai-Yu LeeInstitute of Environmental and Occupational Health Sciences, School of Medicine, National Yang-Ming University, Taipei, Taiwan, ROC.
Chia-Lin LiuGraduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan, ROC.
Yun-Ching ChangDepartment and Graduate School of Pathology, National Defense Medical Center & Tri-Service General Hospital, Taipei, Taiwan, ROC.
Shin NiehDepartment and Graduate School of Pathology, National Defense Medical Center & Tri-Service General Hospital, Taipei, Taiwan, ROC.
Yaoh-Shiang LinDepartment of Otolaryngology-Head and Neck Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, ROC.
Shu-Wen JaoDivision of Colon and Rectum Surgery, Department of Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC.
Su-Feng ChenDepartment of Dental Hygiene, China Medical University, Taichung, Taiwan, ROC.
Tsung-Yun LiuInstitute of Environmental and Occupational Health Sciences, School of Medicine, National Yang-Ming University, Taipei, Taiwan, ROC.
National Defense Medical Center · TWNational Yang Ming Chiao Tung University · TWChina Medical University · TWKaohsiung Veterans General Hospital · TWTri-Service General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A tobacco-specific component, 4-methylnitrosamino-1-3-pyridyl-1-butanone (NNK), is a major risk factor for many cancers. Recent reports have demonstrated that NNK exposure may be associated with tumor progression and chemoresistance in certain cancers. However, the underlying NNK-induced mechanism contributing to the aggressiveness of colorectal cancer (CRC) has not been thoroughly studied. In this study, we used HT29 cells treated with NNK to simulate the long-term exposure of cigarette smoke. A comparative analysis was performed to evaluate cell proliferation, migration, and invasion as well as epithelial-mesenchymal transition (EMT) markers and drug-resistance genes expression, cancer stem cell (CSC) properties, and anti-apoptotic activity. Signaling pathways related to chemoresistance were also investigated. As a result, NNK exposure dose-dependently stimulates cell proliferation, enhance abilities of migration and invasion, induce EMT phenomenon, and attenuate apoptosis. Furthermore, NNK exposure also promotes the capabilities of sphere formation, upregulation of Snail, and overexpression of CD133, Nanog, OCT4, and the drug-resistant genes. Knockdown of Snail results in upregulation of Raf kinase inhibitor protein (RKIP), increased apoptosis, reversal of EMT phenomenon, and reducation of expression of CSC markers, all of which contribute to a decrease of chemoresistance. Our study demonstrates a number of related mechanisms that mediate the effect of NNK exposure on increasing CRC therapeutic resistance via the Snail signaling pathway. Targeting Snail may provide a feasible strategy for the treatment of CRC.

Indexed as

Drug Resistance, NeoplasmAntineoplastic AgentsApoptosisBiomarkers, TumorCarcinogensCell MovementCell ProliferationColorectal NeoplasmsEpithelial-Mesenchymal TransitionHumansNitrosaminesOrganoplatinum CompoundsOxaliplatinPhosphatidylethanolamine Binding ProteinSignal TransductionSnail Family Transcription Factors4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanoneAntineoplastic AgentsBiomarkers, TumorCarcinogensNitrosaminesOrganoplatinum CompoundsOxaliplatinPEBP1 protein, humanPhosphatidylethanolamine Binding ProteinSnail Family Transcription Factorschemoresistancecolorectal cancernicotineNNKSnail

Identifiers

PMID26992205
PMCPMC5029643
OpenAlexW2307214550

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.