Suppression of invasion and metastasis in aggressive salivary cancer cells through targeted inhibition of ID1 gene expression

Murase, Ryuichi; Sumida, Tomoki; Kawamura, Rumi; Onishi-Ishikawa, Akiko; Hamakawa, Hiroyuki; McAllister, Sean D.; Desprez, Pierre Yves

doi:10.1016/j.canlet.2016.04.021

Cited by 20 publications

(8 citation statements)

References 24 publications

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“…ID protein inhibition by a peptide aptamer induces cell cycle arrest and apoptosis in ovarian cancer cells ( Mern et al, 2010a ). Suppression of invasion and metastasis in aggressive salivary and breast cancer cells is targeted through inhibition of ID1 expression ( Fong et al, 2003 ; Murase et al, 2016 ). Inactivation of ID1 genes induces sensitivity of prostate cancer cells to chemotherapeutic drugs ( Wong et al, 2008 ).…”

Section: Current Anticancer Therapeutic Approaches In Agreement With mentioning

confidence: 99%

Similarities Between Embryo Development and Cancer Process Suggest New Strategies for Research and Therapy of Tumors: A New Point of View

Manzo

2019

Front. Cell Dev. Biol.

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Here, I propose that cancer stem cells (CSCs) would be equivalent to para-embryonic stem cells (p-ESCs), derived from adult cells de-re-programmed to a ground state. p-ESCs would differ from ESCs by the absence of genomic homeostasis. A p-ESC would constitute the cancer cell of origin (i-CSC or CSC0), capable of generating an initial tumor, corresponding to a pre-implantation blastocyst. In a niche with proper signals, it would engraft as a primary tumor, corresponding to a post-implantation blastocyst. i-CSC progeny would form primary pluripotent and slow self-renewing CSCs (CSC1s), blocked in an undifferentiated state, corresponding to epiblast cells; CSC1s would be tumor-initiating cells (TICs). CSC1s would generate secondary CSCs (CSC2s), corresponding to hypoblast cells; CSC2s would be tumor growth cells (TGCs). CSC1s/CSC2s would generate tertiary CSCs (CSC3s), with a mesenchymal phenotype; CSC3s would be tumor migrating cells (TMCs), corresponding to mesodermal precursors at primitive streak. CSC3s with more favorable conditions (normoxia), by asymmetrical division, would differentiate into cancer progenitor cells (CPCs), and these into cancer differentiated cells (CDCs), thus generating a defined cell hierarchy and tumor progression, mimicking somito-histo-organogenesis. CSC3s with less favorable conditions (hypoxia) would delaminate and migrate as quiescent circulating micro-metastases, mimicking mesenchymal cells in gastrula morphogenetic movements. In metastatic niches, these CSC3s would install and remain dormant in the presence of epithelial/mesenchymal transition (EMT) signals and hypoxia. But, in the presence of mesenchymal/epithelial transition (MET) signals and normoxia, they would revert to self-renewing CSC1s, reproducing the same cell hierarchy of the primary tumor as macro-metastases. Further similarities between ontogenesis and oncogenesis involving crucial factors, such as ID, HSP70, HLA-G, CD44, LIF, and STAT3, are strongly evident at molecular, physiological and immunological levels. Much experimental data about these factors led to considering the cancer process as ectopic rudimentary ontogenesis, where CSCs have privileged immunological conditions. These would consent to CSC development in an adverse environment, just like an embryo, which is tolerated, accepted and favored by the maternal organism in spite of its paternal semi-allogeneicity. From all these considerations, novel research directions, potential innovative tumor therapy and prophylaxis strategies might, theoretically, result.

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Section: Current Anticancer Therapeutic Approaches In Agreement With mentioning

confidence: 99%

Similarities Between Embryo Development and Cancer Process Suggest New Strategies for Research and Therapy of Tumors: A New Point of View

Manzo

2019

Front. Cell Dev. Biol.

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“…Down-regulation of ID1 expression leads to a significant reduction in lung metastasis in mice injected intravenously with ACCM cells. 22…”

Section: Etiology and Pathology Of Salivary Tumorsmentioning

confidence: 99%

Current State of Knowledge on Salivary Gland Cancers

2018

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Salivary gland cancers (SGCs), categorized as head and neck cancers (HNCs), constitute about 6% of head and neck cancer diagnoses based on estimate by American Head and Neck Society. Salivary gland tumors originate from different glandular cell types and are thus morphologically diverse. These tumors arise from any of the three major and various minor salivary glands. The incidence of SGCs has slowly increased during the last four decades. The etiology of SGCs is mostly unknown; however, specific gene mutations are associated with certain types of salivary tumors. Treatment options include surgical resection, radiation therapy (RT), chemotherapy, and multimodality therapy. HNC patients treated with RT often develop xerostomia and salivary hypofunction due to damaged salivary glands. In this review, we discuss etiology of SGCs, present findings on the role of autophagy in salivary tumorigenesis, review adverse effects of radiation treatment, and examine remedies for restoration of salivary function.

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“…In short, phytocannabinoids (THC, CBD), ECs and EC analogue (AEA, 2-AG, Met-F-AEA), EC-like substances (OEA, PEA) and EC degradation inhibitors (AA-5HT, URB597, JZL184) showed an inhibitory effect on metastatic infiltration of the lung with previously injected lung carcinoma cells [ 32 , 36 , 90 , 93 , 112 , 113 ]. In addition, inhibitory effects of cannabinoids on breast cancer [ 101 , 102 , 114 ], salivary gland cancer [ 100 ] and melanoma cell metastasis [ 44 ] have been described. Finally, further work showed that JZL184 impairs bone metastasis of osteotropic prostate and breast cancer cells in mice and inhibits metastasis of osteosarcoma cells [ 115 ] and that knockdown of MAGL is associated with reduced lymph node metastasis in MAGL-overexpressing nasopharygeal carcinoma cells [ 116 ].…”

Section: Tumour Cell Invasion and Metastasismentioning

confidence: 99%

Cannabinoids as anticancer drugs: current status of preclinical research

Hinz

Ramer

2022

Br J Cancer

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Drugs that target the endocannabinoid system are of interest as pharmacological options to combat cancer and to improve the life quality of cancer patients. From this perspective, cannabinoid compounds have been successfully tested as a systemic therapeutic option in a number of preclinical models over the past decades. As a result of these efforts, a large body of data suggests that the anticancer effects of cannabinoids are exerted at multiple levels of tumour progression via different signal transduction mechanisms. Accordingly, there is considerable evidence for cannabinoid-mediated inhibition of tumour cell proliferation, tumour invasion and metastasis, angiogenesis and chemoresistance, as well as induction of apoptosis and autophagy. Further studies showed that cannabinoids could be potential combination partners for established chemotherapeutic agents or other therapeutic interventions in cancer treatment. Research in recent years has yielded several compounds that exert promising effects on tumour cells and tissues in addition to the psychoactive Δ9-tetrahydrocannabinol, such as the non-psychoactive phytocannabinoid cannabidiol and inhibitors of endocannabinoid degradation. This review provides an up-to-date overview of the potential of cannabinoids as inhibitors of tumour growth and spread as demonstrated in preclinical studies.

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Suppression of invasion and metastasis in aggressive salivary cancer cells through targeted inhibition of ID1 gene expression

Cited by 20 publications

References 24 publications

Similarities Between Embryo Development and Cancer Process Suggest New Strategies for Research and Therapy of Tumors: A New Point of View

Similarities Between Embryo Development and Cancer Process Suggest New Strategies for Research and Therapy of Tumors: A New Point of View

Current State of Knowledge on Salivary Gland Cancers

Cannabinoids as anticancer drugs: current status of preclinical research

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