Evidence map›Paper›PMID 29048616›Full record

ArticleInternational journal of oncology2017

The receptor for activated protein kinase C promotes cell growth, invasion and migration in cervical cancer.

Shan Liao, Songshu Xiao, Hongxiang Chen, Manying Zhang, Zhifang Chen, Yuehua Long, Lu Gao, Junyu He, Yanshan Ge, Wei Yi and 3 more

Abstract read
In one paragraph

Article in International journal of oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
  2. Review
  3. RACK1 promotes the occurrence and progression of cervical carcinoma.Journal of clinical laboratory analysis · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. OncoTargets and therapy · 2018
    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

13 authors.

Shan LiaoHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, P.R. China.
Songshu XiaoDepartment of Gynecology and Obstetrics, The Third Xiangya Hospital, Central South University, Changsha, Hunan, P.R. China.
Hongxiang ChenThe Gynecology Department, People's Hospital of Xinjiang, Urumchi, Xinjiang, P.R. China.
Manying ZhangHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, P.R. China.
Zhifang ChenThe Gynecology Department, The First Affiliated Hospital of Xinjiang Medical University, Urumchi, Xinjiang, P.R. China.
Yuehua LongHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, P.R. China.
Lu GaoHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, P.R. China.
Junyu HeHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, P.R. China.
Yanshan GeHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, P.R. China.
Wei YiHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, P.R. China.
Minghua WuHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, P.R. China.
Guiyuan LiHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, P.R. China.
Yanhong ZhouHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, P.R. China.

Funding

CSRD VA I01 CX002015
6 · The paper itself

Abstract

Cervical cancer is one of the most common malignant tumors in women all over the world. However, the exact etiology of cervical cancer remains unclear. The receptor for activated protein kinase C (RACK1) is reported to be involved in tumorigenesis and tumor progression. Besides, the prognostic value of RACK1 in several kinds of tumors has been identified. However, there are limited studies on the functional role of RACK1 in cervical cancer. In this study, we tested the expression level of RACK1 by immunohistochemistry and western blot technologies and find that it is upregulated in cervical cancer. Colony formation and CCK8 assays indicate that RACK1 promotes cell proliferation in CaSki cervical cancer cells. While the silence of RACK1 decreases the cell proliferation in CCK8 analysis. β-galactosidase staining suggests that RACK1 decreases cell senescence in cervical cancer cells. Invasion and migration assay show that RACK1 promotes the invasion and migration of cervical cancer cells. Also, when RACK1 was silenced, it exerts the opposite result. Furthermore, the mRNA expression levels of MMP‑3, MMP‑9 and MMP‑10 were upregulated in RACK1‑overexpressed CaSki cells by qPCR analysis. RACK1 also induces S phase accumulation in cell cycle analysis and suppresses cell apoptosis in cervical cancer cells. Flow cytometry analysis of mitochondria functions suggests that RACK1 increases the mitochondrial membrane potential (Δψm) levels to prevent mitochondrial apoptosis in cervical cancer cells. To explore the possible mechanism of RACK1, we tested and found that RACK1 upregulates the expression of NF-κB, cyclin D1 and CDK4 and downregulates the expression of p53, p38, p21 and STAT1 in cervical cancer cells. These results suggest that RACK1 promotes cell growth and invasion and inhibits the senescence and apoptosis in cervical cancer cells probably by affecting the p53 pathway.

Indexed as

CarcinogenesisCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMembrane Potential, MitochondrialNeoplasm InvasivenessNeoplasm ProteinsProtein Kinase CReceptors for Activated C KinaseSignal TransductionTumor Suppressor Protein p53Uterine Cervical NeoplasmsNeoplasm ProteinsProtein Kinase CRACK1 protein, humanReceptors for Activated C KinaseTumor Suppressor Protein p53

Identifiers

PMID29048616
PMCPMC5642390

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.