Colon cancer stem cells: Potential target for the treatment of colorectal cancer

Gupta, Riya; Bhatt, Lokesh Kumar; Johnston, Thomas P.; Prabhavalkar, Kedar

doi:10.1080/15384047.2019.1599660

Cited by 112 publications

(101 citation statements)

References 153 publications

(140 reference statements)

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“…Recently, much has been invested to study the host-microbiota interactions, which can explain, with the concept of dysbiosis (i.e., the perturbation of the balance-eubiosis-of the different microbiota populations inhabiting the human gut), the chronic inflammation responsible of carcinogenesis and tumor progression in the colon [39]. However, as similar to what has already been discussed for the other solid cancers, despite the several advances in prevention, diagnosis, and treatment done in the last years for colon cancer, nearly 50% of patients show tumor recurrence, and in this case too, this can be attributed to the presence of CSCs [40].…”

Section: Top Five Lethal Solid Cancerssupporting

confidence: 56%

Retinoic Acids in the Treatment of Most Lethal Solid Cancers

Costantini

Molinari

Farinon

et al. 2020

JCM

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Although the use of oral administration of pharmacological all-trans retinoic acid (ATRA) concentration in acute promyelocytic leukaemia (APL) patients was approved for over 20 years and used as standard therapy still to date, the same use in solid cancers is still controversial. In the present review the literature about the top five lethal solid cancers (lung, stomach, liver, breast, and colon cancer), as defined by The Global Cancer Observatory of World Health Organization, and retinoic acids (ATRA, 9-cis retinoic acid, and 13-cis retinoic acid, RA) was compared. The action of retinoic acids in inhibiting the cell proliferation was found in several cell pathways and compartments: from membrane and cytoplasmic signaling, to metabolic enzymes, to gene expression. However, in parallel in the most aggressive phenotypes several escape routes have evolved conferring retinoic acids-resistance. The comparison between different solid cancer types pointed out that for some cancer types several information are still lacking. Moreover, even though some pathways and escape routes are the same between the cancer types, sometimes they can differently respond to retinoic acid therapy, so that generalization cannot be made. Further studies on molecular pathways are needed to perform combinatorial trials that allow overcoming retinoic acids resistance.

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Section: Top Five Lethal Solid Cancerssupporting

confidence: 56%

Retinoic Acids in the Treatment of Most Lethal Solid Cancers

Costantini

Molinari

Farinon

et al. 2020

JCM

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“…to maintain the stemness of CSCs. Under specific microenvironmental stimuli, certain cancer cells exhibit plasticity, which enables them to resume proliferation through EMT [121]. For example, Chang et al [122] revealed that the activation of the Hh signaling pathway in the TME can transform common prostate cells into stem cells.…”

Section: Cscs Niche Tme and Drug Resistancementioning

confidence: 99%

Drug resistance and Cancer stem cells

et al. 2021

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Therapy resistance is a major problem when treating cancer patients as cancer cells develop mechanisms that counteract the effect of therapeutic compounds, leading to fit and more aggressive clones that contribute to poor prognosis. Therapy resistance can be both intrinsic and/or acquired. These are multifactorial events, and some are related to factors including adaptations in cancer stem cells (CSCs), epithelial-mesenchymal transition (EMT), deregulation of key signaling pathways, drug efflux through ABC transporters, acquired mutations, evading apoptosis, and activation of DNA damage response among others. Among these factors, CSCs represent the major source of therapy resistance. CSCs are a subset of tumor cells that are capable of self-renewal and multilineage progenitor expansion that are known to be intrinsically resistant to anticancer treatments. Multiple clones of CSCs pre-exist, and some can adopt and expand easily to changes in the tumor microenvironment (TME) and/or in response to radio- and chemotherapy. A combination of both intrinsic and extrinsic factors contributes to CSC-mediated therapy resistance. In this review, we will focus on CSCs and therapy resistance as well as suggest strategies to eliminate CSCs and, therefore, overcome resistance.

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“…Colorectal cancer also presents high tumor recurrence of up to 50% [7]. Evidence showed the presence of cancer stem cells with the ability to self-renew and re-form tumors in the colon with added drug resistance [8]. Additionally, CRC exhibits high metastasis rates, where most CRC tumors are diagnosed through detection of a secondary lesions in the liver or lungs, rather than the primary tumor in the colon itself [9].…”

Section: Introductionmentioning

confidence: 99%

Transcriptomic Analyses Revealed Systemic Alterations in Gene Expression in Circulation and Tumor Microenvironment of Colorectal Cancer Patients

Shaath

Toor

Nair

et al. 2019

Cancers

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Colorectal cancer (CRC) is among the leading causes of cancer-related deaths worldwide, underscoring a need for better understanding of the disease and development of novel diagnostic biomarkers and therapeutic interventions. Herein, we performed transcriptome analyses on peripheral blood mononuclear cells (PBMCs), CRC tumor tissue and adjacent normal tissue from 10 CRC patients and PBMCs from 15 healthy controls. Up regulated transcripts from CRC PBMCs were associated with functions related to immune cell trafficking and cellular movement, while downregulated transcripts were enriched in cellular processes related to cell death. Most affected signaling networks were those involved in tumor necrosis factor (TNF) and interleukin signaling. The expression of selected immune-related genes from the RNA-Seq data were further validated using qRT-PCR. Transcriptome analysis of CRC tumors and ingenuity pathway analysis revealed enrichment in several functional categories related to cellular movement, cell growth and proliferation, DNA replication, recombination and repair, while functional categories related to cell death were suppressed. Upstream regulator analysis revealed activation of ERBB2 and FOXM1 networks. Interestingly, there were 18 common upregulated and 36 common downregulated genes when comparing PBMCs and tumor tissue, suggesting transcriptomic changes in the tumor microenvironment could be reflected, in part, in the periphery with potential utilization as disease biomarkers.

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Colon cancer stem cells: Potential target for the treatment of colorectal cancer

Cited by 112 publications

References 153 publications

Retinoic Acids in the Treatment of Most Lethal Solid Cancers

Retinoic Acids in the Treatment of Most Lethal Solid Cancers

Drug resistance and Cancer stem cells

Transcriptomic Analyses Revealed Systemic Alterations in Gene Expression in Circulation and Tumor Microenvironment of Colorectal Cancer Patients

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