Evidence map›Paper›PMID 33042398›Full record

ArticleAmerican journal of translational research2020

SiRNA targeting PFK1 inhibits proliferation and migration and enhances radiosensitivity by suppressing glycolysis in colorectal cancer.

Rui-Fang Tian, Xiao-Fei Li, Cong Xu, Hui Wu, Lan Liu, Li-Hui Wang, Dong He, Ke Cao, Pei-Guo Cao, John K Ma and 1 more

Abstract read
In one paragraph

Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Review
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  7. Phosphofructokinase-1 in Cancer: A Promising Target for Diagnosis and Therapy.Recent patents on anti-cancer drug discovery · 2025
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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

11 authors.

Rui-Fang TianDepartment of Oncology, The Third Xiangya Hospital, Central South University Changsha 410013, Hunan, China.
Xiao-Fei LiDepartment of Oncology, The Third Xiangya Hospital, Central South University Changsha 410013, Hunan, China.
Cong XuDepartment of Oncology, The Third Xiangya Hospital, Central South University Changsha 410013, Hunan, China.
Hui WuDepartment of Oncology, The Third Xiangya Hospital, Central South University Changsha 410013, Hunan, China.
Lan LiuDepartment of Oncology, The Third Xiangya Hospital, Central South University Changsha 410013, Hunan, China.
Li-Hui WangDepartment of Oncology, The Third Xiangya Hospital, Central South University Changsha 410013, Hunan, China.
Dong HeDepartment of Respiratory, The Second People's Hospital of Hunan Province Changsha 410013, Hunan, China.
Ke CaoDepartment of Oncology, The Third Xiangya Hospital, Central South University Changsha 410013, Hunan, China.
Pei-Guo CaoDepartment of Oncology, The Third Xiangya Hospital, Central South University Changsha 410013, Hunan, China.
John K MaCotton O'Neil Cancer Center, Stormont Vail Hospital Topeka, KS, USA.
Cheng-Hui HuangDepartment of Oncology, The Third Xiangya Hospital, Central South University Changsha 410013, Hunan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThis study explored the effects of phosphofructokinase-1 (PFK1) on the radiosensitivity of colorectal cancer (CRC) in vivo and in vitro and the underlying mechanisms.

methodsTissue samples from 48 patients with rectal cancer who had received neoadjuvant radiotherapy followed by surgery were analyzed. The expression of PFK1 in tissue samples was semi-quantitated by immunohistochemistry, and its relationship with clinicopathological features was analyzed. The effects of PFK1 knockdown on the survival, apoptosis, migration, and radiosensitivity of CRC cells were evaluated. Glycolysis-related indicators were used to examine glycolytic activity. The effects of PFK1 on the radiosensitivity of CRC in vivo were assessed by measuring tumor formation in nude mice.

resultsPFK1 was overexpressed in rectal cancer and was higher in radiation-resistant tumors than in radiation-sensitive tumors. SiRNA-induced PFK1 silencing increased apoptosis and inhibited migration and proliferation of CRC cells. Knockdown of PFK1 made the CRC cells sensitive to ionizing radiation in vivo. Oligomycin partially restored the expression of PFK1, enhanced glycolysis, and reversed the enhanced radiosensitivity of CRC cells induced by siRNA-PFK1. Downregulation of PFK1 combined with irradiation inhibited growth of nude mice xenografts, which was related to an increase in apoptosis.

conclusionsOur study indicates that high expression of PFK1 is negatively correlated with radiosensitivity in CRC and likely accelerates the proliferation and migration of CRC cells. Downregulation of PFK1 may enhance the radiosensitivity of CRC cells in vivo and in vitro by inhibiting glycolysis.

Indexed as

Colorectal cancerHCT116 cellsHT29 cellsoligomycin Aphosphofructokinase-1radiotherapy

Identifiers

PMID33042398
PMCPMC7540104

What OpenQuestion holds

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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.