Evidence map›Paper›PMID 33677646›Full record

ArticleClinical and experimental medicine2021

REC8 promotes tumor migration, invasion and angiogenesis by targeting the PKA pathway in hepatocellular carcinoma.

Jing Han, Yun Bai, Jia Wang, Xiao-Li Xie, Ai-di Li, Qian Ding, Zi-Jin Cui, Jie Yin, Xiao-Yu Jiang, Hui-Qing Jiang

Abstract read
PubMed Publisher
In one paragraph

Article in Clinical and experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Jing HanDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, Hebei Clinical Research Center for Digestive Diseases, No. 215, Heping West Road, Shijiazhuang, 050000, Hebei, China.
Yun BaiDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, Hebei Clinical Research Center for Digestive Diseases, No. 215, Heping West Road, Shijiazhuang, 050000, Hebei, China.
Jia WangDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, Hebei Clinical Research Center for Digestive Diseases, No. 215, Heping West Road, Shijiazhuang, 050000, Hebei, China.
Xiao-Li XieDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, Hebei Clinical Research Center for Digestive Diseases, No. 215, Heping West Road, Shijiazhuang, 050000, Hebei, China.
Ai-di LiDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, Hebei Clinical Research Center for Digestive Diseases, No. 215, Heping West Road, Shijiazhuang, 050000, Hebei, China.
Qian DingDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, Hebei Clinical Research Center for Digestive Diseases, No. 215, Heping West Road, Shijiazhuang, 050000, Hebei, China.
Zi-Jin CuiDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, Hebei Clinical Research Center for Digestive Diseases, No. 215, Heping West Road, Shijiazhuang, 050000, Hebei, China.
Jie YinDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, Hebei Clinical Research Center for Digestive Diseases, No. 215, Heping West Road, Shijiazhuang, 050000, Hebei, China.
Xiao-Yu JiangDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, Hebei Clinical Research Center for Digestive Diseases, No. 215, Heping West Road, Shijiazhuang, 050000, Hebei, China.
Hui-Qing JiangDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, Hebei Clinical Research Center for Digestive Diseases, No. 215, Heping West Road, Shijiazhuang, 050000, Hebei, China. jianghq@aliyun.com.ORCID http://orcid.org/0000-0002-5235-1457
Hebei Medical University · CN

Funding

National Natural Science Foundation of China 81602529, 81702324 and 81770601Natural Science Foundation of Hebei Province H2018206176 and H2017206141
6 · The paper itself

Abstract

REC8 is a member of the cohesin family, and its abnormal activation has been detected in cancer cells. This study explored the role and possible mechanism of REC8 in hepatocellular carcinoma (HCC). A total of 40 pairs of HCC and adjacent tissues were collected, and the clinical significance of REC8 expression in HCC was evaluated. REC8 expression in human HCC tissues and HCC cell lines was investigated by quantitative real-time PCR, Western blotting, immunohistochemistry and immunofluorescence staining. The biological functions of REC8 in HCC cell lines were detected by wound-healing assay, Matrigel invasion assay and tube formation assay. The proteins interacting with REC8 were identified by mass spectrometry after immunoprecipitation screening. There was a correlation between the high expression of REC8 and positive alpha-fetoprotein levels. The expression level of REC8 protein in HCC tissues was higher than that in adjacent tissues. REC8 has mainly located in the nucleus of HCC tissue cells and HCC cell lines, but it was expressed in the cytoplasm of adjacent normal tissue cells and hepatocytes. The results of wound healing, transwell invasion and tubular formation assays indicated that the overexpression of REC8 accelerated the metastasis of HCC in vitro; however, metastasis was suppressed after REC8 was silenced by small interference RNA. A total of 57 differentially expressed proteins were identified by mass spectrometry, and it was found that REC8 and PKA RII-α staining was colocalized in the nucleus. The expression levels of MMP-9 and VEGF-C were decreased after treatment with the PKA inhibitor H89. Overall, REC8 promotes the migration, invasion and angiogenesis of HCC cells through the PKA pathway.

Indexed as

alpha-FetoproteinsCarcinoma, HepatocellularCell Cycle ProteinsCell Line, TumorCell MovementCell NucleusCell ProliferationCyclic AMP-Dependent Protein KinasesCytoplasmFemaleGene Expression Regulation, NeoplasticHep G2 CellsHumansLiver NeoplasmsMaleNeoplasm InvasivenessAFP protein, humanalpha-FetoproteinsCell Cycle ProteinsCyclic AMP-Dependent Protein KinasesREC8 protein, humanAngiogenesisHepatocellular carcinomaInvasionMigrationREC8

Identifiers

PMID33677646
OpenAlexW3135417064

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.