Evidence map›Paper›PMID 36504892›Full record

ArticleAmerican journal of cancer research2022

Decreased APOC1 expression inhibited cancer progression and was associated with better prognosis and immune microenvironment in esophageal cancer.

Qiang Guo, Xiao-Li Liu, Ni Jiang, Wen-Jun Zhang, Shao-Wen Guo, Heng Yang, Yan-Mei Ji, Jun Zhou, Jia-Long Guo, Jun Zhang and 1 more

Abstract read
In one paragraph

Article in American journal of cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

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

  1. Pooled it
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  12. APOC1 promotes the progression of osteosarcoma by binding to MTCH2.Experimental and therapeutic medicine · 2023
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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

11 authors.

Qiang GuoDepartment of Cardiothoracic Surgery, Taihe Hospital, Hubei University of Medicine Shiyan, Hubei, China.
Xiao-Li LiuDepartment of Ultrasound, The People's Hospital of Jianyang City Jianyang, Sichuan, China.
Ni JiangDepartment of Obstetrics and Gynecology, Women and Children's Hospital of Chongqing Medical University Chongqing, China.
Wen-Jun ZhangDepartment of Medical Ultrasound, Taihe Hospital, Hubei University of Medicine Shiyan, Hubei, China.
Shao-Wen GuoDepartment of Medical Ultrasound, Taihe Hospital, Hubei University of Medicine Shiyan, Hubei, China.
Heng YangDepartment of Cardiothoracic Surgery, Taihe Hospital, Hubei University of Medicine Shiyan, Hubei, China.
Yan-Mei JiDepartment of Critical Care Medicine, Taihe Hospital, Hubei University of Medicine Shiyan, Hubei, China.
Jun ZhouDepartment of Cardiothoracic Surgery, Taihe Hospital, Hubei University of Medicine Shiyan, Hubei, China.
Jia-Long GuoDepartment of Cardiothoracic Surgery, Taihe Hospital, Hubei University of Medicine Shiyan, Hubei, China.
Jun ZhangDepartment of Cardiothoracic Surgery, Taihe Hospital, Hubei University of Medicine Shiyan, Hubei, China.
Hua-Song LiuDepartment of Cardiothoracic Surgery, Taihe Hospital, Hubei University of Medicine Shiyan, Hubei, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several studies have demonstrated the involvement of apolipoprotein C1 (APOC1) in multiple cancers. However, the role of APOC1 in esophageal cancer (ESCA) has not been elucidated. Hence, we examined the expression of APOC1 in ESCA tissues acquired from The Cancer Genome Atlas (TCGA) database and clinical samples from our hospital. An investigation of the association of APOC1 with the clinicopathological characteristics, prognosis, and diagnosis of ESCA was carried out on the basis of survival, receiver operating characteristics, and correlation analyses. Gene ontology, KEGG analysis, and protein-protein interaction network showed that co-expressed APOC1 genes were involved in the functions, mechanisms, and action network. The effects of APOC1 expression on ESCA cells were explored using CCK-8, migration and invasion assays. The relationship between APOC1 expression and ESCA immune-infiltrating cells and cell markers were examined using correlation analysis. We found that APOC1 was overexpressed in TCGA ESCA tissues and the same was validated in clinical ESCA tissues, with the area under the curve for APOC1 being 0.887. Overexpression of APOC1 was associated with short overall survival, disease-specific survival, progression-free interval, T stage, pathological stage, body mass index, and histological grade. Inhibition of APOC1 expression significantly reduced the proliferation, migration, and invasion of ESCA cells. Furthermore, APOC1 expression positively correlated with the ESTIMATE, immune, and stromal scores in ESCA. Overexpression of APOC1 correlated with the tumor purity, B cells, T helper cells, natural killer cells, cytotoxic cells, and other immune cells. Moreover, APOC1 was involved in ESCA progression via T cell receptor, B cell receptor, and other immune signaling pathways. Thus, APOC1 overexpression is expected to be a biomarker for dismal prognosis and diagnosis of ESCA. Inhibition of APOC1 expression significantly reduced the proliferation, migration, and invasion of ESCA cells. Overexpression of APOC1 was associated with the immune microenvironment in ESCA. Thus, APOC1 may be an efficient biomarker for proper prognosis and diagnosis of ESCA.

Indexed as

APOC1biomarkerESCAimmune microenvironmentprognosis

Identifiers

PMID36504892
PMCPMC9729889

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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.