Evidence map›Paper›PMID 36289466›Full record

ArticleBMC cancer2022

Liver-specific lncRNA FAM99A may be a tumor suppressor and promising prognostic biomarker in hepatocellular carcinoma.

Meile Mo, Xiaoyun Ma, Yihuan Luo, Chao Tan, Bihu Liu, Peng Tang, Qian Liao, Shun Liu, Hongping Yu, Dongping Huang and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 25% of its field
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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. Hypoxia-Induced Suppression of FAM99A and FAM99B Contributes to the Development and Glucose Metabolic Reprogramming of Hepatocellular Carcinoma.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
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  6. Review
  7. Article
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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

12 authors at 3 institutions in 1 country.

Meile Mo *Department of Epidemiology, School of Public Health, Guangxi Medical University, Nanning, Guangxi, 530021, P.R. China.
Xiaoyun Ma *Department of Epidemiology, School of Public Health, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250012, P.R. China.
Yihuan Luo *Department of Acute Care Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, 530021, P.R. China.
Chao TanDepartment of Epidemiology and Statistics, School of Public Health, Guilin Medical University, Guilin, Guangxi, 541004, P.R. China.
Bihu LiuDepartment of Epidemiology, School of Public Health, Guangxi Medical University, Nanning, Guangxi, 530021, P.R. China.
Peng TangDepartment of Epidemiology, School of Public Health, Guangxi Medical University, Nanning, Guangxi, 530021, P.R. China.
Qian LiaoDepartment of Epidemiology, School of Public Health, Guangxi Medical University, Nanning, Guangxi, 530021, P.R. China.
Shun LiuDepartment of Maternal, Child and Adolescent Health, School of Public Health, Guangxi Medical University, Nanning, Guangxi, 530021, P.R. China.
Hongping YuGuangxi Medical University Cancer Hospital, Nanning, Guangxi, 530021, P.R. China.
Dongping HuangDepartment of Sanitary Chemistry, School of Public Health, Guangxi Medical University, Nanning, Guangxi, 530021, P.R. China.
Xiaoyun ZengDepartment of Epidemiology, School of Public Health, Guangxi Medical University, Nanning, Guangxi, 530021, P.R. China. zengxiaoyun@gxmu.edu.cn.
Xiaoqiang QiuDepartment of Epidemiology, School of Public Health, Guangxi Medical University, Nanning, Guangxi, 530021, P.R. China. xqqiu9999@163.com.
Guangxi Medical University · CNGuilin Medical University · CNShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreasing evidence shows that liver-specific long non-coding RNAs (lncRNAs) play important roles in the development of hepatocellular carcinoma (HCC). We identified a novel liver-specific lncRNA, FAM99A, and examined its clinical significance and biological functions in HCC.

methodsThe expression level and clinical value of FAM99A in HCC were examined using The Cancer Genome Atlas (TCGA), International Cancer Genome Consortium (ICGC), and Gene Expression Omnibus (GEO) databases, and were further verified using quantitative real-time polymerase chain reaction (qRT-PCR) in our HCC cohort. Univariate and multivariate Cox proportional hazards regression models were also applied to identify independent prognostic indicators for HCC patients. Cell counting kit-8, colony formation, and Transwell assays were performed to evaluate the effects of FAM99A on the proliferation, migration, and invasion abilities of HCC cells in vitro. A subcutaneous xenograft tumor model was implemented to determine the effect of FAM99A on the tumor growth of HCC cells in vivo. RNA pull-down and mass spectrometry assays were performed to reveal the potential molecular mechanisms of FAM99A in HCC.

resultsThe three public online databases and qRT-PCR data showed that FAM99A was frequently downregulated in HCC tissues and inversely correlated with microvascular invasion and advanced histological grade of HCC patients. Kaplan-Meier survival analysis indicated that decreased FAM99A was significantly associated with poor overall survival of HCC patients based on TCGA database (P = 0.040), ICGC data portal (P < 0.001), and our HCC cohort (P = 0.010). A multivariate Cox proportional hazards regression model based on our HCC cohort suggested that FAM99A was an independent prognostic factor of overall survival for HCC patients (hazard ratio: 0.425, P = 0.039). Upregulation of FAM99A suppressed the proliferation, colony formation, migration, and invasion capacities of HCC cells in vitro, and knockdown of FAM99A had the opposite effects. A subcutaneous xenograft tumor model demonstrated that overexpression of FAM99A significantly inhibited the tumor growth of HCC cells in vivo. Seven tumor-related proteins (PCBP1, SRSF5, SRSF6, YBX1, IGF2BP2, HNRNPK, and HNRNPL) were recognized as possible FAM99A-binding proteins by the RNA pull-down and mass spectrometry assays.

conclusionOur results suggest that FAM99A exerts cancer-inhibiting effects on HCC progression, and it may be a promising prognostic indicator for HCC patients.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsRNA, Long NoncodingBiomarkersCell ProliferationGene Expression Regulation, NeoplasticHumansPhosphoproteinsPrognosisRNA-Binding ProteinsSerine-Arginine Splicing FactorsBiomarkersIGF2BP2 protein, humanPhosphoproteinsRNA-Binding ProteinsRNA, Long NoncodingSerine-Arginine Splicing FactorsSRSF6 protein, humanFAM99AHepatocellular carcinomaLiver-specific lncRNAPrognosisTumor growth

Identifiers

PMID36289466
PMCPMC9609286
OpenAlexW4307657754

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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.