Role of β-catenin in cisplatin resistance, relapse and prognosis of head and neck squamous cell carcinoma

S, Roy; Kar, Madhabananda; Roy, Shomereeta; Saha, Arka; Padhi, Swatishree; Banerjee, Birendranath

doi:10.1007/s13402-017-0365-1

Cited by 35 publications

(27 citation statements)

References 35 publications

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“…The cell viability of parental SCC‐131 cells, p38‐inhibited SCC‐131 cells, parental Cal27 cells, and p38‐inhibited Cal27 cells after cisplatin treatment was assessed by MTT assay as reported earlier …”

Section: Methodsmentioning

confidence: 99%

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Role of p38 MAPK in disease relapse and therapeutic resistance by maintenance of cancer stem cells in head and neck squamous cell carcinoma

Roy

Kar

et al. 2018

J Oral Pathology Medicine

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Section: Methodsmentioning

confidence: 99%

“…Colony forming capacity of parental SCC‐131 cells, p38‐inhibited SCC‐131 cells, parental Cal27 cells and p38‐inhibited Cal27 was performed by clonogenic assay as previously reported …”

Section: Methodsmentioning

confidence: 99%

Role of p38 MAPK in disease relapse and therapeutic resistance by maintenance of cancer stem cells in head and neck squamous cell carcinoma

Roy

Kar

et al. 2018

J Oral Pathology Medicine

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“…It has been confirmed that the reduction in membranous β-catenin was associated with invasive growth, higher risk of lymph node metastasis and shorter survival [13,34,46,47]. The higher level of cytoplasmic/nuclear β-catenin delocalization detected in the surgical margin correlated with higher recurrence rate [48]. Depending on the study, the nuclear expression of β-catenin was observed in 23% of pharyngeal tumors [49], 43% of laryngeal tumors [40], 33% of tongue carcinomas [50], 78% of tongue carcinomas [51] and 17% of HPV-negative oropharyngeal carcinomas [52].…”

Section: Introductionmentioning

confidence: 83%

“…This was mediated by the activation of the Wnt pathway [133]. In the same manner, the induction of Wnt signaling by the inhibition of GSK-3β using lithium chloride led to enhanced DNA repair, evasion of apoptosis and cisplatin resistance [48]. The acquired cisplatin resistance in tongue cancer cells was associated with the induction of WNT-2B and GLUT1 overexpression, and the knockdown of WNT-2B sensitized resistant cells to cisplatin treatment and reduced colony formation in vitro and tumor growth in vivo [134].…”

Section: Functional Significance Of Wnt/β-catenin Pathway Dysregulationmentioning

confidence: 91%

“…WNT ligands overexpression translocation of β-catenin lymph node invasion [61][62][63][64] APC mutational loss stabilization of β-catenin enhanced cell growth [10][11][12][13][14][15][16] FAT1 mutational loss reduced sequestration of β-catenin enhanced cell growth, loss of cell adhesion [60] CDH1 (epi)mutational loss release of β-catenin from cell-cell junctions enhanced cell growth, loss of cell adhesion [51,55,57,58] EGFR overexpression stabilization and nuclear translocation of β-catenin enhanced cell proliferation [13,18] c-MET overexpression Wnt activation via FZD8 increased stemness [99] SFRP1-5 epigenetic silencing reduced Wnt ligand sequestration worse prognosis [73] invasiveness, lymph node metastasis, recurrence, dedifferentiation [26,28,38,42,[44][45][46][47][48]…”

Section: Drivers Of Wnt Activationmentioning

confidence: 99%

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The Significance of the Dysregulation of Canonical Wnt Signaling in Head and Neck Squamous Cell Carcinomas

Paluszczak

2020

Cells

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The knowledge about the molecular alterations which are found in head and neck squamous cell carcinomas (HNSCC) has much increased in recent years. However, we are still awaiting the translation of this knowledge to new diagnostic and therapeutic options. Among the many molecular changes that are detected in head and neck cancer, the abnormalities in several signaling pathways, which regulate cell proliferation, cell death and stemness, seem to be especially promising with regard to the development of targeted therapies. Canonical Wnt signaling is a pathway engaged in the formation of head and neck tissues, however it is not active in adult somatic mucosal cells. The aim of this review paper is to bring together significant data related to the current knowledge on the mechanisms and functional significance of the dysregulation of the Wnt/β-catenin pathway in head and neck tumors. Research evidence related to the role of Wnt signaling activation in the stimulation of cell proliferation, migration and inhibition of apoptosis in HNSCC is presented. Moreover, its role in promoting stemness traits in head and neck cancer stem-like cells is described. Evidence corroborating the hypothesis that the Wnt signaling pathway is a very promising target of novel therapeutic interventions in HNSCC is also discussed.Cells 2020, 9, 723 2 of 20 blocking the interaction between PD-1 receptor and PD-L1, may be beneficial in patients with advanced, metastatic or recurrent HNSCC [7]. However, other therapeutic options are also necessary for the better clinical management of HNSCC patients. To that end, molecular alterations observed in HNSCC need to be studied in detail, in order to point to promising drug targets. Mechanisms of Wnt/β-Catenin Pathway Activation in HNSCCRecent genomic analyses have shown the prevalence of genetic driver alterations in HNSCC, which most frequently affect genes associated with receptor tyrosine kinase (e.g., EGFR, MET, KIT), PI3K, p53, Notch or Hippo signaling pathways. On the other hand, genetic alterations in genes related to canonical Wnt signaling were rarely detected in HNSCC [8,9]. In contrast to colorectal cancers, which show molecular alterations driving Wnt signaling activation in around 90% of cases [9], HNSCC were shown to lack CTNNB1 mutations and APC mutations were present infrequently [10][11][12][13][14][15][16]. The mutations of FAT1 tumor suppressor, which encodes a protocadherin protein that binds and inactivates β-catenin, were detected in some cases of HNSCC [17]. However, the activation of the Wnt/β-catenin pathway in HNSCC seems to be more prevalent than it is suggested by genetic findings, due to cross-talk with other molecular alterations, which can lead to pathway cross-activation. Indeed, it has been shown that β-catenin can be activated via enhanced EGFR or PI3K signaling, which belong to the most frequently dysregulated signaling pathways in HNSCC. In this regard, elevated EGFR expression was associated with delocalized β-catenin expression [13]. In another study, the nuclear ...

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Free radical stress induces DNA damage response in RAW264.7 macrophages during Mycobacterium smegmatis infection

et al. 2018

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Role of β-catenin in cisplatin resistance, relapse and prognosis of head and neck squamous cell carcinoma

Abstract: From our results we conclude that β-catenin may contribute to HNSCC therapy resistance and disease relapse. As such, β-catenin may be explored as a therapeutic target along with conventional therapeutics.

Cited by 35 publications

References 35 publications

Role of p38 MAPK in disease relapse and therapeutic resistance by maintenance of cancer stem cells in head and neck squamous cell carcinoma

Role of p38 MAPK in disease relapse and therapeutic resistance by maintenance of cancer stem cells in head and neck squamous cell carcinoma

The Significance of the Dysregulation of Canonical Wnt Signaling in Head and Neck Squamous Cell Carcinomas

Free radical stress induces DNA damage response in RAW264.7 macrophages during Mycobacterium smegmatis infection

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