Evidence map›Paper›PMID 31278880›Full record

ArticleCancer science2019

Effects of metformin and phenformin on apoptosis and epithelial-mesenchymal transition in chemoresistant rectal cancer.

Ji-Hye Park, Young-Heon Kim, Eun Hyeh Park, Sun-Joo Lee, Hyewon Kim, Areumnuri Kim, Seung Bum Lee, Sehwan Shim, Hyosun Jang, Jae Kyung Myung and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 2 pooled it
3.9field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 2 syntheses or guidelines pooled it, 83 citations in OpenAlex.

  1. Pooled it
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  15. Cells · 2023
    Article
  16. Article
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  18. Metformin inhibits the development and metastasis of colorectal cancer.Medical oncology (Northwood, London, England) · 2022
    Article
  19. Article
  20. Review
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 at 1 institution in 1 country.

Ji-Hye ParkLaboratory of Radiation Exposure & Therapeutics, National Radiation Emergency Medical Center, Korea Institute of Radiological & Medical Science, Seoul, Korea.ORCID https://orcid.org/0000-0003-0674-5110
Young-Heon KimLaboratory of Radiation Exposure & Therapeutics, National Radiation Emergency Medical Center, Korea Institute of Radiological & Medical Science, Seoul, Korea.ORCID https://orcid.org/0000-0002-4766-3181
Eun Hyeh ParkLaboratory of Radiation Exposure & Therapeutics, National Radiation Emergency Medical Center, Korea Institute of Radiological & Medical Science, Seoul, Korea.
Sun-Joo LeeLaboratory of Experimental Pathology, Department of Pathology, Korea Institute of Radiological & Medical Science, Seoul, Korea.
Hyewon KimLaboratory of Experimental Pathology, Department of Pathology, Korea Institute of Radiological & Medical Science, Seoul, Korea.
Areumnuri KimLaboratory of Radiation Exposure & Therapeutics, National Radiation Emergency Medical Center, Korea Institute of Radiological & Medical Science, Seoul, Korea.
Seung Bum LeeLaboratory of Radiation Exposure & Therapeutics, National Radiation Emergency Medical Center, Korea Institute of Radiological & Medical Science, Seoul, Korea.
Sehwan ShimLaboratory of Radiation Exposure & Therapeutics, National Radiation Emergency Medical Center, Korea Institute of Radiological & Medical Science, Seoul, Korea.
Hyosun JangLaboratory of Radiation Exposure & Therapeutics, National Radiation Emergency Medical Center, Korea Institute of Radiological & Medical Science, Seoul, Korea.
Jae Kyung MyungLaboratory of Radiation Exposure & Therapeutics, National Radiation Emergency Medical Center, Korea Institute of Radiological & Medical Science, Seoul, Korea.ORCID https://orcid.org/0000-0001-9612-5323
Sunhoo ParkLaboratory of Radiation Exposure & Therapeutics, National Radiation Emergency Medical Center, Korea Institute of Radiological & Medical Science, Seoul, Korea.
Su-Jae LeeDepartment of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea.
Min Jung KimLaboratory of Radiation Exposure & Therapeutics, National Radiation Emergency Medical Center, Korea Institute of Radiological & Medical Science, Seoul, Korea.
Korea Institute of Radiological and Medical Sciences · KR

Funding

Korea Institute of Radiological and Medical Sciences (KIRAMS)Ministry of Science and ICT (MSIT), Korea 50476-2018Ministry of Science and ICT (MSIT), Korea 50535-2019
6 · The paper itself

Abstract

Recurrence and chemoresistance in colorectal cancer remain important issues for patients treated with conventional therapeutics. Metformin and phenformin, previously used in the treatment of diabetes, have been shown to have anticancer effects in various cancers, including breast, lung and prostate cancers. However, their molecular mechanisms are still unclear. In this study, we examined the effects of these drugs in chemoresistant rectal cancer cell lines. We found that SW837 and SW1463 rectal cancer cells were more resistant to ionizing radiation and 5-fluorouracil than HCT116 and LS513 colon cancer cells. In addition, metformin and phenformin increased the sensitivity of these cell lines by inhibiting cell proliferation, suppressing clonogenic ability and increasing apoptotic cell death in rectal cancer cells. Signal transducer and activator of transcription 3 and transforming growth factor-β/Smad signaling pathways were more activated in rectal cancer cells, and inhibition of signal transducer and activator of transcription 3 expression using an inhibitor or siRNA sensitized rectal cancer cells to chemoresistant by inhibition of the expression of antiapoptotic proteins, such as X-linked inhibitor of apoptosis, survivin and cellular inhibitor of apoptosis protein 1. Moreover, metformin and phenformin inhibited cell migration and invasion by suppression of transforming growth factor β receptor 2-mediated Snail and Twist expression in rectal cancer cells. Therefore, metformin and phenformin may represent a novel strategy for the treatment of chemoresistant rectal cancer by targeting signal transducer and activator of transcription 3 and transforming growth factor-β/Smad signaling.

Indexed as

AnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisCell Line, TumorCell MovementCell ProliferationChemoradiotherapyColonColonic NeoplasmsDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionFluorouracilHumansMaleMetforminMiceFluorouracilMetforminPhenforminSmad ProteinsSTAT3 protein, humanSTAT3 Transcription FactorTransforming Growth Factor betachemoresistant rectal cancermetforminphenforminphosphorylated-signal transducer and activator of transcription 3 (Ser-727)transforming growth factor β receptor type 2

Identifiers

PMID31278880
PMCPMC6726705
OpenAlexW2955745348

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.