Cited by 57Cancer, Hypoxia, and MetabolismMetabolism, Diabetes, and CancerBiochemical and Molecular Research

Regulation of 6-phosphofructo-1-kinase activity in ras-transformed rat-1 fibroblasts

Kole, Hemanta K., Resnick, Ross J., Van Doren, Mark, Racker, Efraim·1991·Archives of Biochemistry and Biophysics

Abstract

Fructose 2,6-bisphosphate (F-2,6-P2) stimulated glycolysis in cell-free extracts of both normal and ras-transfected rat-1 fibroblasts. The extract of the transformed cell glycolyzed more rapidly in both the absence and the presence of F-2,6-P2 than the extract of the parent fibroblast. Addition of mitochondrial ATPase (F1) or inorganic phosphate (Pi) further stimulated lactate production in both cell lines. F-2,6-P2 stimulated the 6-phosphofructo-1-kinase (PFK-1) activity in extracts of normal and transfected cells. The activity in extracts of transformed cells tested with a fructose 6-phosphate regenerating system was considerably higher than in the extract of normal cells. Stimulation of PFK-1 activity by cAMP of both cell lines was not as pronounced as that by F-2,6-P2. In the absence of F-2,6-P2 the PFK-1 activity was strongly inhibited in the transformed cell by ATP concentrations higher than 1 mM, whereas in the normal cell only a marginal inhibition was noted even at 2 or 3 mM ATP. F-2,6-P2 reversed the inhibition of PFK-1 by ATP. Nicotinamide adenine dinucleotide (NAD) at 100 microM (in the presence of 2 mM ATP and 1 microM F-2,6-P2) stimulated PFK-1 activity only in the transformed cell, whereas nicotinamide adenine dinucleotide phosphate (NADP) inhibited PFK-1 activity (in the presence or absence of 1 microM F-2,6-P2) in extracts of both cell lines. No previous observations of stimulation or inhibition by NAD or NADP on PFK-1 activity appear to have been reported. A threefold increase in the intracellular concentration of F-2,6-P2 was observed after transfection of rat-1 fibroblast by the ras oncogene. We conclude from these data that the PFK-1 activity of ras-transfected rat-1 fibroblasts shows a greater response to certain stimulating and inhibitory regulating factors than that of the parent cell.

Integrity signals

Registry

Crossref · 10.1016/0003-9861(91)90084-v

Cites

20 of 20 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Oncogenic KRAS upregulates PFK1, ENO1, and LDHA, promoting glycolytic flux and production of intermediates that can enter anabolic pathways.

    “Oncogenic KRAS also upregulates expression of other key glycolytic enzymes, such as PFK1, ENO1, and LDHA28,31–33, thereby promoting glycolytic flux and enabling the production of glycolytic intermediates that can be shunted into other anabolic pathways (Fig 2).”

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Kole, H. K., Resnick, R. J., Van Doren, M., & Racker, E.
Affiliations
Cornell University (US)
Corresponding author
Racker, Efraim
Venue
Archives of Biochemistry and Biophysics
Publisher
Elsevier BV
Published
1991-05
Volume
286
Issue
2
Pages
586-590
ISSN
0003-9861 (ISSN-L)
OpenAlex
W1973601236
Cited by
57
References
20
Citations by year
2025: 1 · 2024: 1 · 2023: 4 · 2022: 2 · 2021: 3 · 2020: 1 · 2019: 1 · 2018: 4 · 2017: 2 · 2016: 1 · 2015: 4 · 2014: 1 · 2013: 1 · 2012: 3
FWCI
0.42
Type
journal article
Language
en
Open access
closed
Locations
  • Archives of Biochemistry and Biophysics (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01ca008964-26)
  • National Cancer Institute (CA-08964)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Biochemical and Molecular Research
Keywords
6-phosphofructokinase, fructose-2,6-bisphosphate, oncogenic Ras, ras-transformed fibroblasts, Rat-1 fibroblasts, glycolysis regulation, ATP inhibition, NAD+, NADPH, cyclic AMP, lactic acid production, enzyme regulation
MeSH terms
Animals, Cell Line, Cell Transformation, Neoplastic, Cell-Free System, Fibroblasts, Fructose, Fructosediphosphates, Glycolysis, Kinetics, Lactates, Phosphates, Phosphofructokinase-1, Genes, ras, Rats

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review