Evidence map›Paper›PMID 35567291›Full record

ArticleJournal of cellular and molecular medicine2022

MIF/SCL3A2 depletion inhibits the proliferation and metastasis of colorectal cancer cells via the AKT/GSK-3β pathway and cell iron death.

Guan Huang, Lili Ma, Lan Shen, Yan Lei, Lili Guo, Yongjian Deng, Yanqing Ding

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 32 citations in OpenAlex.

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  10. Animals : an open access journal from MDPI · 2024
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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

7 authors at 3 institutions in 1 country.

Guan HuangDepartment of Pathology, Nanfang Hospital and School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Lili MaDepartment of Pathology, Nanfang Hospital and School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Lan ShenDepartment of Pathology, Nanfang Hospital and School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Yan LeiDepartment of Pathology, Nanfang Hospital and School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Lili GuoDepartment of Pathology, Nanfang Hospital and School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Yongjian DengDepartment of Pathology, Nanfang Hospital and School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Yanqing DingDepartment of Pathology, Nanfang Hospital and School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID 0000-0002-3868-3877
Nanfang Hospital · CNKey Laboratory of Guangdong Province · CNLonggang Central Hospital · CN

Funding

Basic Research Project of Knowledge Innovation Program of Shenzhen Science and Technology Innovation Committee JCYJ20160427103041724General Program of National Natural Science Foundation of China 81672453Natural Science Foundation of Guangdong Province 2018A030310433Shenzhen Science, Technology and Innovation Commission Basic Research Project JCYJ20180507181527806
6 · The paper itself

Abstract

This study investigated the mechanisms of migration inhibitory factor (MIF) and solute carrier family 3 member 2 (SLC3A2) in colorectal cancer progression. The levels of MIF and SLC3A2 expression in cells were measured by RT-qPCR. SW480 and SW620 cells were transfected with sh-MIF and sh-SLC3A2, respectively. MIF, SLC3A2, GPX4, E-cadherin and N-cadherin expression were detected by immunofluorescence (IF). CCK8 and Transwell assays were performed to detect cell proliferation and migration. Co-immunoprecipitation (CoIP) was used to measure the binding activity of MIF and SLC3A2. Finally, a nude mouse tumorigenicity assay was used to confirm the functions of MIF and SLC3A2 in colorectal cancer. Results showed that the levels of MIF and SLC3A2 expression were up-regulated in colorectal cancer cells. Inhibition of MIF or SLC3A2 expression prevented cell proliferation, migration, epithelial-mesenchymal transition (EMT) and invasion. In addition, knockdown of MIF and SLC3A2 promoted iron death in SW480 and SW620 cells. CoIP results showed that MIF and SLC3A2 directly interact with each other. Knockdown of both MIF and SLC3A2 inhibited tumour growth and metastasis via the AKT/GSK-3β pathway in vivo. The Akt/GSK-3β pathway was found to participate in regulating MIF and SLC3A2 both in vivo and in vitro. MIF and SLC3A2 might be potential biomarkers for monitoring the treatment of colorectal cancer.

Indexed as

Colorectal NeoplasmsGlycogen Synthase Kinase 3 betaIronMacrophage Migration-Inhibitory FactorsProto-Oncogene Proteins c-aktAnimalsCell DeathCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionMiceSignal TransductionGlycogen Synthase Kinase 3 betaIronMacrophage Migration-Inhibitory FactorsProto-Oncogene Proteins c-aktAkt/GSK-3β signallingcolorectal cancermacrophage migration inhibitory factorSLC3A2

Identifiers

PMID35567291
PMCPMC9189354
OpenAlexW4280623443

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.