Evidence map›Paper›PMID 40074843›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2025

Potential prognostic biomarker of OSBPL10 in pan-cancer associated with immune infiltration.

Jiapeng Qi, Kun Yu, Bei Liu, Yan Wang, Wei Wang, Ran An, Chaojun Wang, Na Li, Dongqian Xu, Lin Liu

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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

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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

2 citing papers in PubMed.

  1. Article
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4 · The record

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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.

Jiapeng Qi *Department of Biochemistry and Molecular Biology, College of Pharmacy, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, 050200, People's Republic of China.
Kun Yu *Engineering Information Department Experimental Center, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, 050200, People's Republic of China.
Bei Liu *Department of Histology and Embryology, College of Integrative Chinese and Western Medicine, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, 050200, People's Republic of China.
Yan WangDepartment of Medical Nursing, College of Nursing, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, 050200, People's Republic of China.
Wei WangDepartment of Biochemistry and Molecular Biology, College of Pharmacy, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, 050200, People's Republic of China.
Ran AnDepartment of Biochemistry and Molecular Biology, College of Pharmacy, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, 050200, People's Republic of China.
Chaojun WangDepartment of Biochemistry and Molecular Biology, College of Pharmacy, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, 050200, People's Republic of China.
Na LiDepartment of Oncology, Hebei General Hospital, Shijiazhuang, Hebei, 050017, People's Republic of China. ln81420@126.com.
Dongqian XuDepartment of Biochemistry and Molecular Biology, College of Pharmacy, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, 050200, People's Republic of China. winterian@126.com.
Lin LiuDepartment of Biochemistry and Molecular Biology, College of Pharmacy, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, 050200, People's Republic of China. liulin1234@163.com.

Funding

Hebei Province Health Department 20231563Hebei Traditional Chinese Medicine Administration 2024084 and 2022080Science and Technology Project of Hebei Education Department QN2022092This research was supported by the Natural Science Foundation of Hebei Province H2023423028Yanzhao Medical Research Project YZZY2023002
6 · The paper itself

Abstract

Oxysterol binding protein-related protein 10 (OSBPL10) is a crucial sterol transporter that plays a significant role in regulating metabolic homeostasis. Previous studies have indicated that OSBPL10 promotes the development of several tumors. However, an integrative bioinformatics and immune infiltration analysis of OSBPL10 across various cancers has yet to be conducted. In this study, we comprehensively analyzed the expression patterns, prognostic value, genetic variations, protein modifications, immune infiltration characteristics, and biological functions of OSBPL10 in 33 human cancers using bioinformatics methods and publicly available databases, including TCGA, GEPIA2, GTEx, UCSC, UALCAN, HPA and TISCH2.0. The function of OSBPL10 and its associated mechanisms were confirmed in the pancreatic cancer cell lines Panc-1 and Mia PaCa-2. Our results revealed that OSBPL10 mRNA expression was significantly upregulated in 12 types of tumor tissues and downregulated in 3 cancers, which was notably associated with poor prognosis, pathological stage, and subtype in 10 tumors. Additionally, the level of promoter methylation exhibited a significant negative correlation with OSBPL10 mRNA expression. OSBPL10 expression was found to be dramatically associated with the levels of chemokines, chemokine receptors, immune checkpoints, and immune cell infiltration across various tumors by activating cancer pathways related to the extracellular matrix (ECM) and TSC/mTOR while downregulating tumor cell stemness. Furthermore, elevated OSBPL10 expression was negatively correlated with most drug sensitivities. In vitro experiments showed that OSBPL10 promoted the proliferation and migration of pancreatic cancer cells through the VEGF/AKT signaling pathway. In conclusion, our pan-cancer analysis suggests that OSBPL10 may serve as a critical biomarker for improving prognosis through OSBPL10-targeted therapies, immunotherapies, and chemotherapeutic combinations in cancer patients.

Indexed as

Biomarkers, TumorNeoplasmsCell Line, TumorGene Expression Regulation, NeoplasticHumansOxysterol Binding ProteinsPancreatic NeoplasmsPrognosisBiomarkers, TumorOxysterol Binding ProteinsDrug sensitivityImmune infiltrationOSBPL10Pan-cancerTSC/mTOR signaling pathwayTumor cell stem

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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.