Evidence map›Paper›PMID 39171598›Full record

ReviewRecent patents on anti-cancer drug discovery2025

Phosphofructokinase-1 in Cancer: A Promising Target for Diagnosis and Therapy.

Ali Raza Ishaq, Tahira Younis, Shankun Lin, Muhammad Usman, Tingfang Wang, Zhe-Sheng Chen

Abstract readReview
PubMed Publisher
In one paragraph

Review in Recent patents on anti-cancer drug discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Review
  2. Role of histone modifications in gastric cancer (Review).International journal of oncology · 2026
    Review
  3. Review
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  6. Article
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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.

Ali Raza IshaqState Key Laboratory of Biocatalysis and Enzyme Engineering, Environmental Microbial Technology Center of Hubei Province, College of Life Science, Hubei University, 430062, Wuhan, China.ORCID 0000-0003-2467-2496
Tahira YounisDepartment of Biochemistry and Biotechnology, The Women University of Multan, Punjab, Pakistan.ORCID 0000-0002-3140-9330
Shankun LinDepartment of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, New York, USA.
Muhammad UsmanDepartment of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, New York, USA.
Tingfang WangShanghai Engineering Research Center of Organ Repair, School of Medicine, Shanghai University, Shanghai, 200444, China.
Zhe-Sheng ChenDepartment of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, New York, USA.

Funding

Baoshan Zhaohui New Drug R&D and Transformation Functional Platform 2021-HSD-8-6-001
6 · The paper itself

Abstract

Tumor cells have distorted enzymatic houses, which change the metabolic state from oxidative phosphorylation to glycolysis with high lactate levels in a hypoxic environment. Redrafting the metabolic profile is an emerging hallmark of cancer. Glycolytic enzyme amplification occurs in about 70% of all malignancies. Current studies have found that PFK-1 overexpression is linked to cell migration, proliferation, and Overall Survival (OS) rate in various human cancer cell lines. This review intended to uncover the bona fide therapeutic target for cancer therapy and elucidate the role of PFK-1 in cancer. Furthermore, this review has outlined the listed pharmacological and genetic inhibitors of PFK-1. Following this review, future studies on PFK-1 should emphasize the molecular pathways implicated in PFK-1 overexpression in cancer development. The terms "PFK-1", "PFKP-1", "PFKL-1", "PFKM-1", "PFKM-1 and cancer", "PFKP-1 and cancer", "PFKL-1 and cancer", and "inhibitors of PFK-1" were used to retrieve the information from a variety of databases, including PubMed, Scopus, Google Scholar, and ScienceDirect. In a variety of malignancies, inhibiting the expression of PFK-1 isoforms has been reported to be the most effective therapeutic method. Overexpression of PFK-1 isoforms induces the Warburg effect, cell proliferation, and carcinogenesis by downregulating apoptotic proteins, such as active caspase-3, caspase-9, and caspase-8. YY1, synoviolin, Sh-RNA-507, SNAI, miR-520a/b/e, miR-128, and β-miR-6517 are some of the putative genetic inhibitors against PFK-1 that have been used to manage the development of malignancies. Pharmacological inhibitors, such as penfluridol, synoviolin/HRD1, quercetin, ginsenoside 20(S)-Rg3, triptolide, worenine, acetylsalicylic acid, and salicylic acid, can regulate the advancement of malignancies by inhibiting PFK-1. Thus, PFK-1 is a promising molecular biomarker for cancer treatment. A prospective investigation can validate the unbiased approaches for discovering brandnew PFK-1 inhibitors for cancer treatment.

Indexed as

Antineoplastic AgentsNeoplasmsPhosphofructokinase-1AnimalsGlycolysisHumansMolecular Targeted TherapyPatents as TopicAntineoplastic AgentsPhosphofructokinase-1cancergenetic inhibitorsPFK-1pharmacologic inhibitors.therapeutic targetstumor progression

Identifiers

PMID39171598

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.