| Literature DB >> 33572433 |
Marta Woźniak1, Gabriela Pastuch-Gawołek2,3, Sebastian Makuch1, Jerzy Wiśniewski4,5, Tibor Krenács6, Peter Hamar7, Andrzej Gamian5, Wiesław Szeja2, Danuta Szkudlarek1, Monika Krawczyk2,3, Siddarth Agrawal1,8.
Abstract
Methotrexate (MTX) is a commonly used antimetabolite, which inhibits folate and DNA synthesis to be effective in the treatment of various malignancies. However, MTX therapy is hindered by the lack of target tumor selectivity. We have designed, synthesized and evaluated a novel glucose-methotrexate conjugate (GLU-MTX) both in vitro and in vivo, in which a cleavable linkage allows intracellular MTX release after selective uptake through glucose transporter-1 (GLUT1). GLU-MTX inhibited the growth of colorectal (DLD-1), breast (MCF-7) and lung (A427) adenocarcinomas, squamous cell carcinoma (SCC-25), osteosarcoma (MG63) cell lines, but not in WI-38 healthy fibroblasts. In tumor cells, GLU-MTX uptake increased 17-fold compared to unconjugated MTX. 4,6-O-ethylidene-α-D-glucose (EDG), a GLUT1 inhibitor, significantly interfered with GLU-MTX induced growth inhibition, suggesting a glucose-mediated drug uptake. Glu-MTX also caused significant tumor growth delay in vivo in breast cancer-bearing mice. These results show that our GLUT-MTX conjugate can be selectively uptake by a range of tumor cells to cause their significant growth inhibition in vitro, which was also confirmed in a breast cancer model in vivo. GLUT1 inhibitor EDG interfered with these effects verifying the selective drug uptake. Accordingly, GLU-MTX offers a considerable tumor selectivity and may offer cancer growth inhibition at reduced toxicity.Entities:
Keywords: Warburg effect; anticancer drugs; cancer treatment; drug design and discovery; glucose metabolism; glycoconjugates; methotrexate; targeted therapy
Year: 2021 PMID: 33572433 PMCID: PMC7916191 DOI: 10.3390/ijms22041748
Source DB: PubMed Journal: Int J Mol Sci ISSN: 1422-0067 Impact factor: 5.923