Evidence map›Paper›PMID 27536070›Full record

ArticleDrug design, development and therapy2016

Endoplasmic reticulum stress-induced autophagy determines the susceptibility of melanoma cells to dabrafenib.

Chao Ji, Ziping Zhang, Lihong Chen, Kunli Zhou, Dongjun Li, Ping Wang, Shuying Huang, Ting Gong, Bo Cheng

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Drug design, development and therapy, 2016. 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 It has been retracted, and should not be counted.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 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-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

8 citing papers in PubMed, 16 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Chao JiDepartment of Dermatology, the 1st Affiliated Hospital of Fujian Medical University; Fujian Institute of Dermatology and Venereology, Fujian Medical University, Fuzhou, Fujian, People's Republic of China.
Ziping ZhangDepartment of Dermatology, the 1st Affiliated Hospital of Fujian Medical University; Fujian Institute of Dermatology and Venereology, Fujian Medical University, Fuzhou, Fujian, People's Republic of China.
Lihong ChenDepartment of Dermatology, the 1st Affiliated Hospital of Fujian Medical University; Fujian Institute of Dermatology and Venereology, Fujian Medical University, Fuzhou, Fujian, People's Republic of China.
Kunli ZhouDepartment of Dermatology, the 1st Affiliated Hospital of Fujian Medical University; Fujian Institute of Dermatology and Venereology, Fujian Medical University, Fuzhou, Fujian, People's Republic of China.
Dongjun LiDepartment of Dermatology, the 1st Affiliated Hospital of Fujian Medical University; Fujian Institute of Dermatology and Venereology, Fujian Medical University, Fuzhou, Fujian, People's Republic of China.
Ping WangDepartment of Dermatology, the 1st Affiliated Hospital of Fujian Medical University; Fujian Institute of Dermatology and Venereology, Fujian Medical University, Fuzhou, Fujian, People's Republic of China.
Shuying HuangDepartment of Dermatology, the 1st Affiliated Hospital of Fujian Medical University; Fujian Institute of Dermatology and Venereology, Fujian Medical University, Fuzhou, Fujian, People's Republic of China.
Ting GongFujian Institute of Dermatology and Venereology, Fujian Medical University, Fuzhou, Fujian, People's Republic of China.
Bo ChengDepartment of Dermatology, the 1st Affiliated Hospital of Fujian Medical University; Fujian Institute of Dermatology and Venereology, Fujian Medical University, Fuzhou, Fujian, People's Republic of China.
Fujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melanoma is one of the deadliest skin cancers and accounts for most skin-related deaths due to strong resistance to chemotherapy drugs. In the present study, we investigated the mechanisms of dabrafenib-induced drug resistance in human melanoma cell lines A375 and MEL624. Our studies support that both endoplasmic reticulum (ER) stress and autophagy were induced in the melanoma cells after the treatment with dabrafenib. In addition, ER stress-induced autophagy protects melanoma cells from the toxicity of dabrafenib. Moreover, inhibition of both ER stress and autophagy promote the sensitivity of melanoma cells to dabrafenib. Taken together, the data suggest that ER stress-induced autophagy determines the sensitivity of melanoma cells to dabrafenib. These results provide us with promising evidence that the inhibition of autophagy and ER stress could serve a therapeutic effect for the conventional dabrafenib chemotherapy.

Indexed as

Antineoplastic AgentsAutophagyCell DeathCell SurvivalDose-Response Relationship, DrugDrug Resistance, NeoplasmEndoplasmic Reticulum StressHumansImidazolesMelanomaOximesStructure-Activity RelationshipTumor Cells, CulturedAntineoplastic AgentsdabrafenibImidazolesOximesapoptosisautophagydabrafenibER stressmelanoma

Identifiers

PMID27536070
PMCPMC4977101
OpenAlexW2501585900

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.