Evidence map›Paper›PMID 28177895›Full record

ArticleOncotarget2017

Over-expression of Thrombospondin 4 correlates with loss of miR-142 and contributes to migration and vascular invasion of advanced hepatocellular carcinoma.

Fang Su, Jun Zhao, Shukui Qin, Rui Wang, Yumei Li, Qiang Wang, Yi Tan, Hao Jin, Fangquan Zhu, Yurong Ou and 9 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

34 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Pathophysiological roles of thrombospondin-4 in disease development.Seminars in cell & developmental biology · 2024
    Review
  8. Review
  9. Article
  10. Review
  11. DNA Methylation inCancers · 2021
    Article
  12. Article
  13. Extracellular Matrix Biomarkers in Colorectal Cancer.International journal of molecular sciences · 2021
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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

19 authors at 4 institutions in 1 country.

Fang SuDepartment of Medical Oncology, First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui, China.
Jun ZhaoDepartment of General Surgery, Yijishan Hospital of Wannan Medical College, Wuhu 241000, Anhui, China.
Shukui QinDepartment of Medical Oncology, PLA Cancer Center, Nanjing Bayi Hospital, Nanjing 210002, Jiangsu, China.
Rui WangDepartment of Medical Oncology, First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui, China.
Yumei LiDepartment of Medical Oncology, First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui, China.
Qiang WangDepartment of Information Center, Bengbu Medical College, Bengbu 233030, Anhui, China.
Yi TanDepartment of Hepatobiliary Surgery, First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui, China.
Hao JinDepartment of Hepatobiliary Surgery, First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui, China.
Fangquan ZhuDepartment of Hepatobiliary Surgery, First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui, China.
Yurong OuDepartments of Pathology, First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui, China.
Zenong ChengDepartments of Pathology, First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui, China.
Wen SuDepartment of Medical Oncology, First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui, China.
Fuyou ZhaoDepartment of Medical Oncology, First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui, China.
Yan YangDepartment of Medical Oncology, First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui, China.
Zhengguang ZhouDepartment of Medical Oncology, First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui, China.
Jiyue ZhengDepartment of Medical Oncology, First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui, China.
Yawei LiDepartment of Medical Oncology, First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui, China.
Zhongwen LiDepartment of Biologic Science, Bengbu Medical College, Bengbu 233030, Anhui, China.
Qiong WuDepartment of Medical Oncology, First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui, China.
First Affiliated Hospital of Bengbu Medical College · CNBengbu Medical College · CNFirst Affiliated Hospital of Wannan Medical College · CNJiangsu Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is a common malignancy found worldwide and is associated with a high incidence of metastasis and vascular invasion. Elucidating the molecular mechanisms that underlie HCC tumorigenesis and progression is necessary for the development of novel therapeutics. By analyzing the Cancer Genome Atlas Network (TCGA) dataset, we identified Thrombospondin 4 (THBS4) is significantly overexpressed in HCC samples and is correlated with prognosis. Overexpression of THBS4 was also highly correlated with vascular invasion of advanced HCC. While THBS4 is often overexpressed in HCC it has also been shown to inhibit tumor growth by mediating cell-to-cell and cell-to-matrix interactions. Here, we identified that knockdown of THBS4 inhibits migration and invasion of HCC cells and inhibits HCC induced angiogenesis. MiRNAs are crucial regulators of multiple cellular processes, and aberrant expression of miRNAs has been observed to effect cancer development and progression. We further found that miR-142 is an upstream regulator of THBS4 in HCC cells. Moreover, miR-142 was significantly down-regulated in HCC tissue samples and correlated with overexpression of THBS4. Overexpression of miR-142 inhibited invasion and angiogenesis of HCC cells and re-expression of THBS4 overcame these effects of miR-142 expression. Stable over-expression of miR-142 significantly inhibited tumour growth in a xenograft tumour model through inhibiting THBS4 expression and tumor angiogenesis. In conclusion, our findings indicate that loss of miR-142 results in the over-expression of THBS4, which enhances HCC migration and vascular invasion. Thus, targeting THBS4 or miR-142 may provide a promising therapeutic strategy for treatment of advanced HCC.

Indexed as

AnimalsCarcinoma, HepatocellularCell Line, TumorCell MovementCell ProliferationHeterograftsHumansLiver NeoplasmsMiceMicroRNAsNeoplasm InvasivenessSurvival RateThrombospondinsMicroRNAsMIRN142 microRNA, humanthrombospondin 4Thrombospondinshepatocellular carcinomamigrationmiR-142THBS4vascular invasion

Identifiers

PMID28177895
PMCPMC5410303
OpenAlexW2585142060

What OpenQuestion holds

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LicenceCC BY
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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.