Evidence map›Paper›PMID 27313783›Full record

ArticleJournal of Cancer2016

Correlation of GOLPH3 Gene with Wnt Signaling Pathway in Human Colon Cancer Cells.

Cheng-Zhi Qiu, Ming-Zhen Wang, Wai-Shi Yu, Yan-Ta Guo, Chun-Xiao Wang, Xiao-Feng Yang

Open access · goldAbstract read
In one paragraph

Article in Journal of Cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
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  6. Oncogenic Roles of GOLPH3 in the Physiopathology of Cancer.International journal of molecular sciences · 2020
    Review
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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

6 authors at 2 institutions in 1 country.

Cheng-Zhi QiuDepartment of General Surgery, the Second Affiliated Hospital of Fujian Medical University, Quanzhou 362000, Fujian Province, China.
Ming-Zhen WangDepartment of General Surgery, the Second Affiliated Hospital of Fujian Medical University, Quanzhou 362000, Fujian Province, China.
Wai-Shi YuDepartment of General Surgery, the Second Affiliated Hospital of Fujian Medical University, Quanzhou 362000, Fujian Province, China.
Yan-Ta GuoDepartment of General Surgery, the Second Affiliated Hospital of Fujian Medical University, Quanzhou 362000, Fujian Province, China.
Chun-Xiao WangDepartment of General Surgery, the Second Affiliated Hospital of Fujian Medical University, Quanzhou 362000, Fujian Province, China.
Xiao-Feng YangDepartment of General Surgery, the Second Affiliated Hospital of Fujian Medical University, Quanzhou 362000, Fujian Province, China.
Second Affiliated Hospital of Fujian Medical University · CNFujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveOverexpression of GOLPH3 in colorectal cancer tissue may promote cell proliferation and activate the Wnt signaling pathway. We investigated the correlation between GOLPH3 gene expression and the Wnt signaling pathway to explore the mechanism of the overexpression of GOLPH3 gene which promotes proliferation in human colon cancer cells.

methodsWe measured expression of GOLPH3 mRNA in the human colon cancer cell lines HCT116, HT29, SW480 and SW620 by RT-PCR, and the cells with the highest expression were selected and divided into four groups: negative control, GOLPH3 siRNA transfection (siRNA-GOLPH3), Akt inhibitor (Tricinbine), and glycogen synthase kinase (GSK)-3β inhibitor (TWS119). After human colon cancer cells were transfected with siRNA-GOLPH3, we used RT-PCR to investigate the silencing effect of GOLPH3 gene. We assessed the activity of the Wnt signaling pathway in all groups using the Topflash method. Proliferation and apoptosis of colon cancer SW620 cells were detected by MTT assay, colony formation assay and flow cytometry. Expression of Golgi phosphoprotein (GOLPH)3, β-catenin, GSK-3β and pS9-GSK-3β in cancer cells was determined by Western blotting.

resultsSW620 cells expressed the highest level of GOLPH3 mRNA, and the silence effect was good after they were transfected with siRNA-GOLPH3. The relative luminescence units (RLU) values in the experimental groups were significantly lower than in the negative control group (P<0.001). There was no significant difference in the RLU values among the experimental groups (P> 0.05). The growth inhibition ratio and apoptosis rate of cancer cells in each experimental group were significantly higher than those in the control group, and the cell colony count in the experimental group was significantly lower than in the control group (P<0.05). In addition, the RLU value, proliferation and apoptosis rate of cancer cells did not differ significantly between each two experimental groups. Western blotting showed that, compared with the control group, expression of β-catenin and pS9-GSK3 proteins were significantly decreased in the experimental group. Expression of GSK-3β in the experimental group did not different from that of the control group.

conclusionsOverexpression of GOLPH3 gene activated the Wnt signaling pathway, as well as increasing expression of β-catenin, promoting proliferation and inhibiting apoptosis in human colon cancer cells. The mechanism of action was that overexpression of GOLPH3 gene activated Akt, which may also further activate the Wnt signaling pathway via GSK-3β, and promote proliferation in human colon cancer cells.

Indexed as

AktColon cancer cellsglycogen synthase kinase-3βGOLPH3Wnt signaling pathwayβ-catenin.

Identifiers

PMID27313783
PMCPMC4910585
OpenAlexW2407164893

What OpenQuestion holds

Textmetadata
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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.