Evidence map›Paper›PMID 26314859›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

miR-15a enhances the anticancer effects of cisplatin in the resistant non-small cell lung cancer cells.

Vildan Bozok Çetintaş, Aslı Tetik Vardarlı, Zekeriya Düzgün, Burçin Tezcanlı Kaymaz, Eda Açıkgöz, Hüseyin Aktuğ, Buket Kosova Can, Cumhur Gündüz, Zuhal Eroğlu

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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

22 citing papers in PubMed, 40 citations in OpenAlex.

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  6. Insight into autophagy in platinum resistance of cancer.International journal of clinical oncology · 2023
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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

9 authors at 1 institution in 1 country.

Vildan Bozok ÇetintaşDepartment of Medical Biology, Ege University School of Medicine, Izmir, Turkey. vildanbcetintas@gmail.com.
Aslı Tetik VardarlıDepartment of Medical Biology, Ege University School of Medicine, Izmir, Turkey.
Zekeriya DüzgünDepartment of Medical Biology, Ege University School of Medicine, Izmir, Turkey.
Burçin Tezcanlı KaymazDepartment of Medical Biology, Ege University School of Medicine, Izmir, Turkey.
Eda AçıkgözDepartment of Embryology and Histology, Ege University School of Medicine, Izmir, Turkey.
Hüseyin AktuğDepartment of Embryology and Histology, Ege University School of Medicine, Izmir, Turkey.
Buket Kosova CanDepartment of Medical Biology, Ege University School of Medicine, Izmir, Turkey.
Cumhur GündüzDepartment of Medical Biology, Ege University School of Medicine, Izmir, Turkey.
Zuhal EroğluDepartment of Medical Biology, Ege University School of Medicine, Izmir, Turkey.
Ege University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Platinum-based chemotherapies have long been used as a standard treatment in non-small cell lung cancer. However, cisplatin resistance is a major problem that restricts the use of cisplatin. Deregulated cell death mechanisms including apoptosis and autophagy could be responsible for the development of cisplatin resistance and miRNAs are the key regulators of these mechanisms. We aimed to analyse the effects of selected miRNAs in the development of cisplatin resistance and found that hsa-miR-15a-3p was one of the most significantly downregulated miRNAs conferring resistance to cisplatin in Calu1 epidermoid lung carcinoma cells. Only hsa-miR-15a-3p mimic transfection did not affect cell proliferation or cell death, though decreased cell viability was found when combined with cisplatin. We found that induced expression of hsa-miR-15a-3p via mimic transfection sensitised cisplatin-resistant cells to apoptosis and autophagy. Our results demonstrated that the apoptosis- and autophagy-inducing effects of hsa-miR-15a-3p might be due to suppression of BCL2, which exhibits a major connection with cell death mechanisms. This study provides new insights into the mechanism of cisplatin resistance due to silencing of the tumour suppressor hsa-miR-15a-3p and its possible contribution to apoptosis, autophagy and cisplatin resistance, which are the devil's triangle in determining cancer cell fate.

Indexed as

Antineoplastic AgentsApoptosisBlotting, WesternCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationCisplatinDrug Resistance, NeoplasmFluorescent Antibody TechniqueGene Expression Regulation, NeoplasticHumansLung NeoplasmsMicroRNAsReal-Time Polymerase Chain ReactionTransfectionAntineoplastic AgentsCisplatinMicroRNAsMIRN15 microRNA, humanApoptosisAutophagyCisplatin resistancehsa-miR-15a-3pNon-small cell lung cancer

Identifiers

PMID26314859
OpenAlexW1595368585

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.