Cited by 89Drug Transport and Resistance MechanismsCancer Cells and MetastasisPI3K/AKT/mTOR signaling in cancer

Cell signaling and cancer: a mechanistic insight into drug resistance

Panda, Munmun, Biswal, Bijesh K.·2019·Molecular Biology Reports

Abstract

Drug resistance is a major setback for advanced therapeutics in multiple cancers. The increasing prevalence of this resistance is a growing concern and bitter headache for the researchers since a decade. Hence, it is essential to revalidate the existing strategies available for cancer treatment and to look after a novel therapeutic approach for target based killing of cancer cells at the genetic level. This review outlines the different mechanisms enabling resistance including drug efflux, drug target alternation, alternative splicing, the release of the extracellular vesicle, tumor heterogeneity, epithelial-mesenchymal transition, tumor microenvironment, the secondary mutation in the receptor, epigenetic alternation, heterodimerization of receptors, amplification of target and amplification of components rather than the target. Furthermore, existing evidence and the role of various signaling pathways like EGFR, Ras, PI3K/Akt, Wnt, Notch, TGF-β, Integrin-ECM signaling in drug resistance are explained. Lastly, the prevention of this resistance by a contemporary therapeutic strategy, i.e., a combination of specific signaling pathway inhibitors and the cocktail of a cancer drug is summarized showing the new treatment strategies.

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Crossref · 10.1007/s11033-019-04958-6

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157 of 157 references verified0 citation errors · 0 not checkable

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  • Responses to immunotherapy can be considerably delayed and unpredictable, in part due to the cascade of immune events required for a productive anti-tumor cytotoxic response.

    “Rather, responses can be considerably delayed and unpredictable, in part due to the cascade of immune events that are required for a productive anti-tumor cytotoxic response382.”

    From TGFβ biology in cancer progression and immunotherapy (2021) · cites this paper as [382]

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Authors
Panda, M., & Biswal, B. K.
Affiliations
National Institute of Technology Rourkela (IN)
Corresponding author
Biswal, Bijesh K.
Venue
Molecular Biology Reports
Published
2019-07-06
Volume
46
Issue
5
Pages
5645-5659
ISSN
  • 0301-4851 (ISSN-L)
  • 1573-4978
OpenAlex
W2954345285
Cited by
89
References
157
Citations by year
2026: 8 · 2025: 9 · 2024: 7 · 2023: 14 · 2022: 18 · 2021: 21 · 2020: 10 · 2019: 1 · 2018: 1
FWCI
1.19
Type
journal article
Language
en
Open access
closed
Locations
  • Molecular Biology Reports (publishedVersion)
  • PubMed (publishedVersion)
Funders
Department of Science and technology, Science and Engineering Research Board (DST, SERB), New Delhi, India (ECR/2016/000792)
Topics
  • Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
  • Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
Keywords
chemoresistance, signal transduction, drug efflux, drug target alterations, alternative splicing, extracellular vesicles, tumor heterogeneity, epithelial-mesenchymal transition, tumor microenvironment, epigenetic modifications, receptor heterodimerization, gene amplification, EGFR signaling, Ras signaling, PI3K/Akt signaling, Wnt signaling, Notch signaling, TGF-beta signaling, combination therapy, signaling pathway inhibitors
MeSH terms
Antineoplastic Agents, Humans, Neoplasms, Signal Transduction, Genes, erbB-1, Drug Resistance, Neoplasm, Phosphatidylinositol 3-Kinases, MAP Kinase Signaling System, Cell Line, Tumor, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases, Epithelial-Mesenchymal Transition, Tumor Microenvironment, Wnt Signaling Pathway

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