Evidence map›Paper›PMID 41102409›Full record

ArticleNature chemical biology2026

A small molecule targets LIC1 to suppress lung tumor growth by inducing autophagy.

Jia-Luo Huang, Lei-Ming Wu, Shu-Qi Wu, Fang-Yu Yuan, Han-Zhuang Weng, Dong Huang, Lu Gan, Shuo-Bin Chen, Gui-Hua Tang, Sheng Yin

Abstract read
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In one paragraph

Article in Nature chemical biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
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  4. Review
  5. Review
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

10 authors.

Jia-Luo Huang *School of Pharmaceutical Sciences, State Key Laboratory of Oncology in South China, Sun Yat-sen University, Guangzhou, P. R. China.
Lei-Ming Wu *School of Pharmaceutical Sciences, State Key Laboratory of Oncology in South China, Sun Yat-sen University, Guangzhou, P. R. China.
Shu-Qi WuSchool of Pharmaceutical Sciences, State Key Laboratory of Oncology in South China, Sun Yat-sen University, Guangzhou, P. R. China.
Fang-Yu YuanSchool of Pharmaceutical Sciences, State Key Laboratory of Oncology in South China, Sun Yat-sen University, Guangzhou, P. R. China.
Han-Zhuang WengSchool of Pharmaceutical Sciences, State Key Laboratory of Oncology in South China, Sun Yat-sen University, Guangzhou, P. R. China.
Dong HuangSchool of Pharmaceutical Sciences, State Key Laboratory of Oncology in South China, Sun Yat-sen University, Guangzhou, P. R. China.
Lu GanSchool of Pharmaceutical Sciences, State Key Laboratory of Oncology in South China, Sun Yat-sen University, Guangzhou, P. R. China.
Shuo-Bin ChenSchool of Pharmaceutical Sciences, State Key Laboratory of Oncology in South China, Sun Yat-sen University, Guangzhou, P. R. China.
Gui-Hua TangSchool of Pharmaceutical Sciences, State Key Laboratory of Oncology in South China, Sun Yat-sen University, Guangzhou, P. R. China.
Sheng YinSchool of Pharmaceutical Sciences, State Key Laboratory of Oncology in South China, Sun Yat-sen University, Guangzhou, P. R. China. yinsh2@mail.sysu.edu.cn.ORCID 0000-0002-5678-6634

Funding

National Natural Science Foundation of China (National Science Foundation of China) 22407144National Natural Science Foundation of China (National Science Foundation of China) 82273804National Natural Science Foundation of China (National Science Foundation of China) 82304322National Natural Science Foundation of China (National Science Foundation of China) 82404454Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation) 2024A1515010169
6 · The paper itself

Abstract

Small molecules that induce autophagy in specific biological contexts can provide invaluable chemical probes and potential anticancer therapeutics. Here we identified a potent autophagy inducer 3,4-diisobutyryl derivative of auxarthrol A (DAA) from an endophyte-derived small-molecule library. DAA demonstrates notable antitumor efficacy in non-small cell lung cancer (NSCLC) tumor and sensitizes tumors to anti-PD1 immunotherapy. Using a photoaffinity labeling approach, we identified light intermediate chain 1 (LIC1), a subunit of dynein, as the direct target of DAA. We found that LIC1 is overexpressed in NSCLC tumors and correlates with poor survival. Mechanistically, the targeting of LIC1 by DAA markedly disrupts the interactions between LIC1 and stress-sensing effector RuvB-like AAA ATPase 1, which in turn elevates downstream GCN2-eIF2α-ATF4 axis-mediated integrated stress response, ultimately promoting autophagic cell death. Our findings define LIC1 as a novel therapeutic target for NSCLC and highlight the potential of DAA as a promising autophagy inducer for treatment of this disease.

Indexed as

Antineoplastic AgentsAutophagyCarcinoma, Non-Small-Cell LungLung NeoplasmsPyrrolesSmall Molecule LibrariesAnimalsCell Line, TumorCell ProliferationHumansMiceAntineoplastic AgentsPyrrolesSmall Molecule Libraries

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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.