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Phosphofructokinase‐P Modulates P44/42 MAPK Levels in HeLa Cells
Author(s) -
Cardim Pires Thyago Rubens,
Albanese Jamille Mansur,
Schwab Michael,
Marette André,
Carvalho Renato Sampaio,
SolaPenna Mauro,
Zancan Patricia
Publication year - 2017
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.25774
Subject(s) - phosphofructokinase , hela , downregulation and upregulation , mapk/erk pathway , gene silencing , cancer cell , microbiology and biotechnology , glycolysis , cancer research , chemistry , cell , biology , cancer , kinase , biochemistry , enzyme , genetics , gene
It is known that interfering with glycolysis leads to profound modification of cancer cell proliferation. However, energy production is not the major reason for this correlation. Here, using HeLa cells as a model for cancer, we demonstrate that phosphofructokinase‐P (PFK‐P), which is overexpressed in diverse types of cancer including HeLa cells, modulates expression of P44/42 mitogen‐activated protein kinase (MAPK). Silencing of PFK‐P did not alter HeLa cell viability or energy production, including the glycolytic rate. On the other hand, silencing of PFK‐P induced the downregulation of p44/42 MAPK, augmenting the sensitivity of HeLa cells to different drugs. Conversely, overexpression of PFK‐P promotes the upregulation of p44/42 MAPK, making the cells more resistant to the drugs. These results indicate that overexpression of PFK‐P by cancer cells is related to activation of survival pathways via upregulation of MAPK and suggest PFK‐P as a promising target for cancer therapy. J. Cell. Biochem. 118: 1216–1226, 2017. © 2016 Wiley Periodicals, Inc.