Colon cancer: Cancer stem cells markers, drug resistance and treatment

Kozovská, Zuzana; Gabrisova, Veronika; Kučerová, Lucia

doi:10.1016/j.biopha.2014.10.019

Cited by 192 publications

(172 citation statements)

References 76 publications

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“…Treatments were given once a day, 5 d per week. Tumor formation and body weight were assessed every 4 d. Tumor volume (cm 3 ) was recorded by measuring 2 perpendicular diameters of the tumors with the following formula: volume D (length £ width 2 ) / 2. After 16 d of treatment (23 d after cancer cell injection), the mice were sacrificed.…”

Section: Animal Studiesmentioning

confidence: 99%

“…2 The current management of colon cancer relies primarily on surgery (-laparoscopic colectomy) and adjuvant chemotherapy, with or without concurrent irradiation depending on the tumor location and stage. 3 Nevertheless, recurrence and metastasis occur frequently in patients with colon cancer and are associated with low survival rate and poor prognosis. Thus improved treatment strategies are imperative to improving patient outcomes.…”

Section: Introductionmentioning

confidence: 99%

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Methylglyoxal suppresses human colon cancer cell lines and tumor growth in a mouse model by impairing glycolytic metabolism of cancer cells associated with down-regulation of c-Myc expression

Zhou

et al. 2016

Cancer Biology & Therapy

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Methylglyoxal (MG) is a highly reactive dicarbonyl compound exhibiting anti-tumor activity. The antitumor effects of MG have been demonstrated in some types of cancer, but its role in colon cancer and the mechanisms underlying this activity remain largely unknown. We investigated its role in human colon cancer and the underlying mechanism using human colon cancer cells and animal model. Viability, proliferation, and apoptosis were quantified in DLD-1 and SW480 colon cancer cells by using the Cell Counting Kit-8, plate colony formation assay, and flow cytometry, respectively. Cell migration and invasion were assessed by wound healing and transwell assays. Glucose consumption, lactate production, and intracellular ATP production also were assayed. The levels of c-Myc protein and mRNA were quantitated by western blot and qRT-PCR. The anti-tumor role of MG in vivo was investigated in a DLD-1 xenograft tumor model in nude mice. We demonstrated that MG inhibited viability, proliferation, migration, and invasion and induced apoptosis of DLD-1 and SW480 colon cancer cells. Treatment with MG reduced glucose consumption, lactate production, and ATP production and decreased c-Myc protein levels in these cells. Moreover, MG significantly suppressed tumor growth and c-Myc expression in vivo. Our findings suggest that MG plays an anti-tumor role in colon cancer. It inhibits cancer cell growth by altering the glycolytic pathway associated with downregulation of c-Myc protein. MG has therapeutic potential in colon cancer by interrupting cancer metabolism.

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Section: Animal Studiesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Methylglyoxal suppresses human colon cancer cell lines and tumor growth in a mouse model by impairing glycolytic metabolism of cancer cells associated with down-regulation of c-Myc expression

Zhou

et al. 2016

Cancer Biology & Therapy

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“…5 Similarly, CSCs with cancer-initiating properties and partially overlapping surface markers have been identified in colon cancer, leukemia, and other cancers. [7][8][9] CSCs contain mutations that lead to the acquisition of additional properties on top of the tumor-initiating cells' properties described above which are essentially properties of normal tissue stem cells. These mutations endow them with the required abilities for cancer development and maintenance, including sustained proliferation and evasion from growth suppressors, resistance to apoptosis, induction of angiogenesis, invasion and metastasis potential, genome instability, avoidance of immune recognition, and destruction and metabolism adjustments.…”

Section: Introduction: Cancer Stem Cell Theorymentioning

confidence: 99%

Proteasome expression and activity in cancer and cancer stem cells

Voutsadakis

2017

Tumour Biol.

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Proteasome is a multi-protein organelle that participates in cellular proteostasis by destroying damaged or short-lived proteins in an organized manner guided by the ubiquitination signal. By being in a central place in the cellular protein complement homeostasis, proteasome is involved in virtually all cell processes including decisions on cell survival or death, cell cycle, and differentiation. These processes are important also in cancer, and thus, the proteasome is an important regulator of carcinogenesis. Cancers include a variety of cells which, according to the cancer stem cell theory, descend from a small percentage of cancer stem cells, alternatively termed tumor-initiating cells. These cells constitute the subsets that have the ability to propagate the whole variety of cancer and repopulate tumors after cytostatic therapies. Proteasome plays a role in cellular processes in cancer stem cells, but it has been found to have a decreased function in them compared to the rest of cancer cells. This article will discuss the transcriptional regulation of proteasome sub-unit proteins in cancer and in particular cancer stem cells and the relationship of the proteasome with the pluripotency that is the defining characteristic of stem cells. Therapeutic opportunities that present from the understanding of the proteasome role will also be discussed.

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“…One such example is CD133, which has recently been identified as the marker for CSC in lung cancer [120], prostate cancer [121,122,123], brain cancer [124,125,126,127], colon cancer [128,129,130], and hepatic carcinoma [131,132,133,134]. CSCs are also identified as the side population (SP), based on the expression of the ABCG2 protein and the ability to efflux Hoechst dye [135].…”

Section: The Existence Of Cancer Stem Cellsmentioning

confidence: 99%

Mesenchymal Stem Cell Expressing TRAIL as Targeted Therapy against Sensitised Tumour

Fakiruddin

Ghazalli

Lim

et al. 2018

IJMS

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Tapping into the ability of engineered mesenchymal stem cells (MSCs) to mobilise into the tumour has expanded the scope of cancer treatment. Engineered MSCs expressing tumour necrosis factor (TNF)-related apoptosis inducing ligand (MSC-TRAIL) could serve as a platform for an efficient and targeted form of therapy. However, the presence of cancer stem cells (CSCs) that are resistant to TRAIL and apoptosis may represent a challenge for effective treatment. Nonetheless, with the discovery of small molecular inhibitors that could target CSCs and tumour signalling pathways, a higher efficacy of MSC-TRAIL mediated tumour inhibition can be achieved. This might pave the way for a more effective form of combined therapy, which leads to a better treatment outcome. In this review, we first discuss the tumour-homing capacity of MSCs, its effect in tumour tropism, the different approach behind genetically-engineered MSCs, and the efficacy and safety of each agent delivered by these MSCs. Then, we focus on how sensitisation of CSCs and tumours using small molecular inhibitors can increase the effect of these cells to either TRAIL or MSC-TRAIL mediated inhibition. In the conclusion, we address a few questions and safety concerns regarding the utilization of engineered MSCs for future treatment in patients.

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Colon cancer: Cancer stem cells markers, drug resistance and treatment

Cited by 192 publications

References 76 publications

Methylglyoxal suppresses human colon cancer cell lines and tumor growth in a mouse model by impairing glycolytic metabolism of cancer cells associated with down-regulation of c-Myc expression

Methylglyoxal suppresses human colon cancer cell lines and tumor growth in a mouse model by impairing glycolytic metabolism of cancer cells associated with down-regulation of c-Myc expression

Proteasome expression and activity in cancer and cancer stem cells

Mesenchymal Stem Cell Expressing TRAIL as Targeted Therapy against Sensitised Tumour

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