Evidence map›Paper›PMID 28470188›Full record

ArticleScientific reports2017

RGC32 induces epithelial-mesenchymal transition by activating the Smad/Sip1 signaling pathway in CRC.

Xiao-Yan Wang, Sheng-Nan Li, Hui-Fang Zhu, Zhi-Yan Hu, Yan Zhong, Chuan-Sha Gu, Shi-You Chen, Teng-Fei Liu, Zu-Guo Li

Abstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Regulator of Cell Cycle Protein (RGCC/RGC-32) Protects against Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2022
    Article
  4. Article
  5. Article
  6. Targeting the Complement Pathway in Malignant Glioma Microenvironments.Frontiers in cell and developmental biology · 2021
    Review
  7. Article
  8. RGC-32 and diseases: the first 20 years.Immunologic research · 2019
    Review
  9. Role of C5b-9 and RGC-32 in Cancer.Frontiers in immunology · 2019
    Review
  10. 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

9 authors.

Xiao-Yan WangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Sheng-Nan LiDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Hui-Fang ZhuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Zhi-Yan HuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Yan ZhongDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Chuan-Sha GuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Shi-You ChenDepartment of Physiology &Pharmacology, University of Georgia, Athens, GA, United States.
Teng-Fei LiuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Zu-Guo LiDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Response gene to complement 32 (RGC32) is a transcription factor that regulates the expression of multiple genes involved in cell growth, viability and tissue-specific differentiation. However, the role of RGC32 in tumorigenesis and tumor progression in colorectal cancer (CRC) has not been fully elucidated. Here, we showed that the expression of RGC32 was significantly up-regulated in human CRC tissues versus adjacent normal tissues. RGC32 expression was significantly correlated with invasive and aggressive characteristics of tumor cells, as well as poor survival of CRC patients. We also demonstrated that RGC32 overexpression promoted proliferation, migration and tumorigenic growth of human CRC cells in vitro and in vivo. Functionally, RGC32 facilitated epithelial-mesenchymal transition (EMT) in CRC via the Smad/Sip1 signaling pathway, as shown by decreasing E-cadherin expression and increasing vimentin expression. In conclusion, our findings suggested that overexpression of RGC32 facilitates EMT of CRC cells by activating Smad/Sip1 signaling.

Indexed as

Epithelial-Mesenchymal TransitionSignal TransductionAnimalsBiomarkers, TumorCell Cycle ProteinsCell Line, TumorCell MovementCell ProliferationColorectal NeoplasmsFemaleGene Expression Regulation, NeoplasticHumansMaleMice, Inbred BALB CMice, NudeMiddle AgedBiomarkers, TumorCell Cycle ProteinsGEMIN2 protein, humanMuscle ProteinsNerve Tissue ProteinsRGCC protein, humanRNA-Binding ProteinsSmad Proteins

Identifiers

PMID28470188
PMCPMC5415763

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.