The origins of cancer cell dormancy

Morales-Valencia, Jorge; Gourichon, David

doi:10.1016/j.gde.2022.101914

Cited by 15 publications

(8 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Tumor cells are in the proliferation phase of the cell cycle for a long time, and explosive growth after cell dormancy makes tumor treatment difficult. 181 , 182 It was recently found that histone modification could inhibit the transcription of lncRNA miR100HG, thereby inhibiting its role in inducing cell cycle G0-G1 arrest in CRC and promoting cell proliferation. 183 Similar to RNA modifications, m 6 A modifications are also present in DNA.…”

Section: Discussionmentioning

confidence: 99%

RNA Modifications Meet Tumors

Yang¹,

Zhang²,

Xia³

et al. 2022

CMAR

View full text Add to dashboard Cite

RNA modifications occur through the whole process of gene expression regulation, including transcription, translation, and post-translational processes. They are closely associated with gene expression, RNA stability, and cell cycle. RNA modifications in tumor cells play a vital role in tumor development and metastasis, changes in the tumor microenvironment, drug resistance in tumors, construction of tumor cell-cell “internet”, etc. Several types of RNA modifications have been identified to date and have various effects on the biological characteristics of different tumors. In this review, we discussed the function of RNA modifications, including N 6 -methyladenine (m 6 A), 5-methylcytosine (m 5 C), N 7 -methyladenosine (m 7 G), N 1 -methyladenosine (m 1 A), pseudouridine (Ψ), and adenosine-to-inosine (A-to-I), in the microenvironment and therapy of solid and liquid tumors.

show abstract

Section: Discussionmentioning

confidence: 99%

RNA Modifications Meet Tumors

Yang¹,

Zhang²,

Xia³

et al. 2022

CMAR

View full text Add to dashboard Cite

show abstract

“…This means that if there are no more cancer cells and the treatment is stopped, the model is in equilibrium without growth, albeit unstable. This may also represent a state of cancer cell dormancy, an adaptive strategy used by cancer cells to overcome drug cytotoxicity [ 44 ]. This stage may persist until complete metabolism of the drug, which would allow the cell to re-enter the cell cycle and tumor growth to recur.…”

Section: Discussionmentioning

confidence: 99%

Validation of a Mathematical Model Describing the Dynamics of Chemotherapy for Chronic Lymphocytic Leukemia In Vivo

Guzev

Jadhav

Hezkiy

et al. 2022

Cells

View full text Add to dashboard Cite

In recent years, mathematical models have developed into an important tool for cancer research, combining quantitative analysis and natural processes. We have focused on Chronic Lymphocytic Leukemia (CLL), since it is one of the most common adult leukemias, which remains incurable. As the first step toward the mathematical prediction of in vivo drug efficacy, we first found that logistic growth best described the proliferation of fluorescently labeled murine A20 leukemic cells injected in immunocompetent Balb/c mice. Then, we tested the cytotoxic efficacy of Ibrutinib (Ibr) and Cytarabine (Cyt) in A20-bearing mice. The results afforded calculation of the killing rate of the A20 cells as a function of therapy. The experimental data were compared with the simulation model to validate the latter’s applicability. On the basis of these results, we developed a new ordinary differential equations (ODEs) model and provided its sensitivity and stability analysis. There was excellent accordance between numerical simulations of the model and results from in vivo experiments. We found that simulations of our model could predict that the combination of Cyt and Ibr would lead to approximately 95% killing of A20 cells. In its current format, the model can be used as a tool for mathematical prediction of in vivo drug efficacy, and could form the basis of software for prediction of personalized chemotherapy.

show abstract

“…According to previous hypothesis ( Shyh-Chang and Ng, 2017 ), it seems that long-term self-renewing stem cells maintain their multipotent capacity in a hypoxic environment and downregulate mitochondrial activity ( Han et al, 2018 ). Moreover, it has been suggested that in stress conditions cancer cells can suffer a phenotypic transition from a proliferating state to a dormant state characterized by no proliferation, no death, no senescence, resistance to chemotherapy, high expression of dormant markers, metabolic suppression, and recovery to active status ( Morales-Valencia and David, 2022 ). In fact, tumor dormancy is a critical stage in cancer development where cancer cells can remain occult, asymptomatic, and resistant to therapy.…”

Section: Discussionmentioning

confidence: 99%

Metabolic fingerprinting of chemotherapy-resistant prostate cancer stem cells. An untargeted metabolomic approach by liquid chromatography-mass spectrometry

Bort

Sánchez²,

León³

et al. 2022

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Chemoresistance is one of the most important challenges in cancer therapy. The presence of cancer stem cells within the tumor may contribute to chemotherapy resistance since these cells express high levels of extrusion pumps and xenobiotic metabolizing enzymes that inactivate the therapeutic drug. Despite the recent advances in cancer cell metabolism adaptations, little is known about the metabolic adaptations of the cancer stem cells resistant to chemotherapy. In this study, we have undertaken an untargeted metabolomic analysis by liquid chromatography–high-resolution spectrometry combined with cytotoxicity assay, western blot, quantitative real-time polymerase chain reaction (qPCR), and fatty acid oxidation in a prostate cancer cell line resistant to the antiandrogen 2-hydroxiflutamide with features of cancer stem cells, compared to its parental androgen-sensitive cell line. Metabolic fingerprinting revealed 106 out of the 850 metabolites in ESI+ and 67 out of 446 in ESI- with significant differences between the sensitive and the resistant cell lines. Pathway analysis performed with the unequivocally identified metabolites, revealed changes in pathways involved in energy metabolism as well as posttranscriptional regulation. Validation by enzyme expression analysis indicated that the chemotherapy-resistant prostate cancer stem cells were metabolically dormant with decreased fatty acid oxidation, methionine metabolism and ADP-ribosylation. Our results shed light on the pathways underlying the entry of cancer cells into dormancy that might contribute to the mechanisms of drug resistance.

show abstract

The origins of cancer cell dormancy

Cited by 15 publications

References 59 publications

RNA Modifications Meet Tumors

RNA Modifications Meet Tumors

Validation of a Mathematical Model Describing the Dynamics of Chemotherapy for Chronic Lymphocytic Leukemia In Vivo

Metabolic fingerprinting of chemotherapy-resistant prostate cancer stem cells. An untargeted metabolomic approach by liquid chromatography-mass spectrometry

Contact Info

Product

Resources

About