Evidence map›Paper›PMID 26225121›Full record

ArticleCancer cell international2015

Mechanistic attributes of S100A7 (psoriasin) in resistance of anoikis resulting tumor progression in squamous cell carcinoma of the oral cavity.

Kaushik Kumar Dey, Siddik Sarkar, Ipsita Pal, Subhasis Das, Goutam Dey, Rashmi Bharti, Payel Banik, Joygopal Roy, Sukumar Maity, Indranil Kulavi and 1 more

RetractedErratum issuedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Cancer cell international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

10 citing papers in PubMed, 24 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 1 country.

Kaushik Kumar DeySchool of Medical Science and Technology, Indian Institute of Technology, Kharagpur, 721302 West Bengal India.
Siddik SarkarSchool of Medical Science and Technology, Indian Institute of Technology, Kharagpur, 721302 West Bengal India.
Ipsita PalSchool of Medical Science and Technology, Indian Institute of Technology, Kharagpur, 721302 West Bengal India.
Subhasis DasSchool of Medical Science and Technology, Indian Institute of Technology, Kharagpur, 721302 West Bengal India.
Goutam DeySchool of Medical Science and Technology, Indian Institute of Technology, Kharagpur, 721302 West Bengal India.
Rashmi BhartiSchool of Medical Science and Technology, Indian Institute of Technology, Kharagpur, 721302 West Bengal India.
Payel BanikSchool of Medical Science and Technology, Indian Institute of Technology, Kharagpur, 721302 West Bengal India.
Joygopal RoyDr Rafi Ahmed Dental College and Hospital, Kolkata, 700014 West Bengal India.
Sukumar MaityCalcutta Medical College, Kolkata, 700073 West Bengal India.
Indranil KulaviBankura Sammilani Medical College, Bankura, 722101 West Bengal India.
Mahitosh MandalSchool of Medical Science and Technology, Indian Institute of Technology, Kharagpur, 721302 West Bengal India.
Indian Institute of Technology Kharagpur · INBankura Sammilani Medical College · INDr. R. Ahmed Dental College and Hospital · INMedical College and Hospital, Kolkata · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSquamous cell carcinoma of the oral cavity (SCCOC) is the dominant origin of cancer associated mortality. Previous findings by our study reported that acquisition of anoikis resistance has a significant role in tumor progression of oral cavity. Several genes were over-expressed in anoikis-resistant cells under detached conditions which we confirmed earlier by microarray. Normal oral squamous epithelia grow adherent to a basement membrane, and when detached from the extracellular matrix, undergoes programmed cell death. The acquisition of anoikis-resistance is crucial phenomena in oral tumor advancement. In the current study, we have identified S100A7 expression as contributing factor for anoikis resistance and tumorigenicity in human oral cancer cells. Further, we have explored that elevated S100A7 expression in anoikis-sensitive oral keratinocytes and cancer cells reshape them more resistant to anoikis and apoptosis inducers via activation of cellular intrinsic and extrinsic avenue.

methodsA subset of human cancer cell lines TU167, JMAR, JMARC39, JMARC42 and MDA-MB-468 were utilized for the generation of resistant stable cell lines. Further, immunohistochemistry, western blot and immunoprecipitation, assays of apoptosis, soft agar assay, orthotopic animal model and signaling elucidation were performed to establish our hypothesis.

resultsS100A7 gene is found to be responsible for anoikis resistance and tumorigenicity in human oral cancer cells. We have observed up-regulation of S100A7 in anoikis resistant cell lines, orthotropic model and patients samples with head and neck cancer. It is also noticed that secretion of S100A7 protein in conditioned medium by anoikis resistant head & neck cancer cell and in saliva of head and neck cancer patients. Up-regulation of S100A7 expression has triggered enhanced tumorigenicity and anchorage-independent growth of cancer cells through Akt phosphorylation leading to development of aniokis resistance in head and neck cancer cells.

conclusionsThese data have led us to conclude that S100A7 is the major contributing factor in mediating anoikis-resistance of oral cancer cells and local tumor progression, and S100A7 might be useful as diagnostic marker for early detection of primary and recurrent squamous cell cancer.

Indexed as

AnoikisApoptosisCell proliferationPsoriasinS100A7Squamous cell carcinoma

Identifiers

PMID26225121
PMCPMC4518584
OpenAlexW2167804530

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LicenceCC BY
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Registered trials

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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.