Evidence map›Paper›PMID 41145465›Full record

ArticleCell death discovery2025

LINC01198 activates Hippo signaling to stimulate IL-1β autocrine for driving vemurafenib resistance by associating with TAOK1/2 in melanoma.

Jieyu Liu, Xiaoting Liang, Ke Wang, Chunting Zhang, Can Li, Lei Zhao, Yanjie Kuang, Min Wang, Jun Liu, Liang Zhou and 1 more

Abstract read
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In one paragraph

Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Jieyu Liu *Institute of Molecular Immunology, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, China.
Xiaoting Liang *Department of Toxicology, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, China.
Ke Wang *Institute of Molecular Immunology, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, China.
Chunting ZhangDepartment of Occupational Health and Occupational Medicine, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, China.
Can LiDepartment of Toxicology, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, China.
Lei ZhaoDepartment of Toxicology, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, China.
Yanjie KuangDepartment of Toxicology, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, China.
Min WangDepartment of Toxicology, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, China.
Jun LiuDepartment of Toxicology, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, China.
Liang ZhouInstitute of Molecular Immunology, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, China. zhzliang@smu.edu.cn.ORCID http://orcid.org/0000-0001-5973-7873
Li MaInstitute of Molecular Immunology, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, China. mali_61648322@smu.edu.cn.ORCID http://orcid.org/0000-0001-5847-2375

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82272344
6 · The paper itself

Abstract

Vemurafenib (VEM) is an important targeted drug for treating melanoma harboring BRAF-V600E mutation. Despite its remarkable curative efficacy in early clinical treatment, most patients developed drug resistance within one year. Nevertheless, the critical factors driving vemurafenib resistance and mechanisms leading to treatment failure in melanoma are debating and inconclusive. In this study, we established vemurafenib-resistance melanoma cell strain together with acute vemurafenib treatment and characterized LINC01198 as the only one LncRNA up-regulated in both of stable vemurafenib-resistant and acute vemurafenib-treated melanoma cells. Functionally, loss of LINC01198 significantly compromised melanoma resistance against vemurafenib. Mechanistically, LINC01198 directly associates with TAOK1/2 to inhibit TAOK1/2 phosphorylation and thereby elicits Hippo signaling through TAOK/LATS axis, which redistributes YAP/TAZ into nucleus and promotes the expression and secretion of IL-1β to support vemurafenib resistance in melanoma. Our study not only identifies LINC01198 as a potent indicator and critical factor for driving vemurafenib resistance, but also suggests a series of therapeutic targets for tackling vemurafenib resistance in melanoma.

Identifiers

PMID41145465
PMCPMC12559216

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