Evidence map›Paper›PMID 38971819›Full record

ArticleNature communications2024

ATP6V0A1-dependent cholesterol absorption in colorectal cancer cells triggers immunosuppressive signaling to inactivate memory CD8

Tu-Xiong Huang, Hui-Si Huang, Shao-Wei Dong, Jia-Yan Chen, Bin Zhang, Hua-Hui Li, Tian-Tian Zhang, Qiang Xie, Qiao-Yun Long, Yang Yang and 7 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
–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

36 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

17 authors.

Tu-Xiong Huang *Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pharmacology and International Cancer Center, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, China.ORCID 0000-0001-8698-647X
Hui-Si Huang *Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pharmacology and International Cancer Center, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, China.
Shao-Wei DongDepartment of Clinical Medical Research Center, The First Affiliated Hospital of Southern University of Science and Technology (Shenzhen People's Hospital), Shenzhen, 518000, Guangdong, China.
Jia-Yan ChenGuangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pharmacology and International Cancer Center, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, China.
Bin ZhangDepartment of Clinical Medical Research Center, The First Affiliated Hospital of Southern University of Science and Technology (Shenzhen People's Hospital), Shenzhen, 518000, Guangdong, China.ORCID 0000-0002-9264-8554
Hua-Hui LiShenzhen Institute of Advanced Technology (SIAT), Chinese Academy of Sciences (CAS), Shenzhen, 518055, Guangdong, China.
Tian-Tian ZhangGuangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pharmacology and International Cancer Center, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, China.
Qiang XieGuangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pharmacology and International Cancer Center, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, China.
Qiao-Yun LongDepartment of Clinical Medical Research Center, The First Affiliated Hospital of Southern University of Science and Technology (Shenzhen People's Hospital), Shenzhen, 518000, Guangdong, China.
Yang YangGuangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pharmacology and International Cancer Center, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, China.
Lin-Yuan HuangGuangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pharmacology and International Cancer Center, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, China.
Pan ZhaoDepartment of Clinical Medical Research Center, The First Affiliated Hospital of Southern University of Science and Technology (Shenzhen People's Hospital), Shenzhen, 518000, Guangdong, China.
Jiong BiThe First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, Guangdong, China.
Xi-Feng LuClinical Research Center, The First Affiliated Hospital of Shantou University Medical College, Shantou, 515041, Guangdong, China.
Fan PanShenzhen Institute of Advanced Technology (SIAT), Chinese Academy of Sciences (CAS), Shenzhen, 518055, Guangdong, China.ORCID 0009-0008-6325-0089
Chang ZouDepartment of Clinical Medical Research Center, The First Affiliated Hospital of Southern University of Science and Technology (Shenzhen People's Hospital), Shenzhen, 518000, Guangdong, China. zouchang@cuhk.edu.cn.ORCID 0009-0007-5992-0257
Li FuGuangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pharmacology and International Cancer Center, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, China. gracelfu@szu.edu.cn.ORCID 0000-0003-2643-6278

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82173003
6 · The paper itself

Abstract

Obesity shapes anti-tumor immunity through lipid metabolism; however, the mechanisms underlying how colorectal cancer (CRC) cells utilize lipids to suppress anti-tumor immunity remain unclear. Here, we show that tumor cell-intrinsic ATP6V0A1 drives exogenous cholesterol-induced immunosuppression in CRC. ATP6V0A1 facilitates cholesterol absorption in CRC cells through RAB guanine nucleotide exchange factor 1 (RABGEF1)-dependent endosome maturation, leading to cholesterol accumulation within the endoplasmic reticulum and elevated production of 24-hydroxycholesterol (24-OHC). ATP6V0A1-induced 24-OHC upregulates TGF-β1 by activating the liver X receptor (LXR) signaling. Subsequently, the release of TGF-β1 into the tumor microenvironment by CRC cells activates the SMAD3 pathway in memory CD8

Indexed as

CD8-Positive T-LymphocytesCholesterolColorectal NeoplasmsSignal TransductionTransforming Growth Factor beta1AnimalsCarbamatesCell Line, TumorHumansHydroxycholesterolsImmunologic MemoryLiver X ReceptorsMiceMice, Inbred C57BLPyrrolidinesSmad3 ProteinCarbamatesCholesterolHydroxycholesterolsLiver X ReceptorsPyrrolidinesSmad3 ProteinTransforming Growth Factor beta1Vacuolar Proton-Translocating ATPases

Identifiers

PMID38971819
PMCPMC11227557

What OpenQuestion holds

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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.