Evidence map›Paper›PMID 33520360›Full record

ArticleAmerican journal of cancer research2021

Radiation engenders converse migration and invasion in colorectal cancer cells through opposite modulation of ANXA2/AKT/GSK3β pathway.

Han Pan, Yimeng Song, Hang Zhang, Yang Bai, Teruaki Konishi, Alisa Kobayashi, Chunlin Shao, Yan Pan

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2021. 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
0.6field-weighted citation impact, top 34% 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

10 citing papers in PubMed, 9 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

8 authors at 1 institution in 1 country.

Han PanInstitute of Radiation Medicine, Shanghai Medical College, Fudan University No. 2094 Xie-Tu Road, Shanghai 200032, China.
Yimeng SongInstitute of Radiation Medicine, Shanghai Medical College, Fudan University No. 2094 Xie-Tu Road, Shanghai 200032, China.
Hang ZhangInstitute of Radiation Medicine, Shanghai Medical College, Fudan University No. 2094 Xie-Tu Road, Shanghai 200032, China.
Yang BaiInstitute of Radiation Medicine, Shanghai Medical College, Fudan University No. 2094 Xie-Tu Road, Shanghai 200032, China.
Teruaki KonishiInstitute for Quantum Life Science, National Institutes for Quantum and Radiological Science and Technology Inage, Chiba 263-8555, Japan.
Alisa KobayashiInstitute for Quantum Life Science, National Institutes for Quantum and Radiological Science and Technology Inage, Chiba 263-8555, Japan.
Chunlin ShaoInstitute of Radiation Medicine, Shanghai Medical College, Fudan University No. 2094 Xie-Tu Road, Shanghai 200032, China.
Yan PanInstitute of Radiation Medicine, Shanghai Medical College, Fudan University No. 2094 Xie-Tu Road, Shanghai 200032, China.
Shanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Radiation therapy is an effective non-surgical means to achieve local control for various solid tumors including colorectal cancer (CRC), but metastasis and recurrences after conventional radiotherapy remains a major obstacle in clinical practice, and the knowledge concerning the changes of metastatic potential after heavy ion radiation is still limited. This study investigated how radiation, including γ- and carbon ion radiation, would change the metastatic capacity of two CRC cell lines, HCT116 and DLD-1, and examined the underlying molecular mechanisms. We found that the migration and invasion was enhanced in DLD-1 cells but impaired in HCT116 cells in vitro and in vivo after radiation of γ-rays or carbons, and radiation induced epithelial mesenchymal transition (EMT) in DLD-1 cells but mesenchymal epithelial transition (MET) in HCT116 cells. The expression of snail, a key inducer of EMT, was significantly enhanced by inhibition of glycogen synthase kinase-3β (GSK3β) in both cell lines, suggesting the modulation of snail was alike in the two CRC cell lines. However, radiation inactivated GSK3β through stimulating the phosphorylation of AKT and GSK3β at Ser473 and Ser9 in DLD-1 cells respectively, but activated GSK3β by decreasing the expression of pAKT

Indexed as

ANXA2/GSK3βColorectal cancer cellsEMTmigration and invasionradiation

Identifiers

PMID33520360
PMCPMC7840724
OpenAlexW3126767586

What OpenQuestion holds

Textmetadata
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.