A loss of profilin‐1 in late‐stage oral squamous cell carcinoma

Adami, Guy R.; O'Callaghan, Thomas N.; Kolokythas, Antonia; Cabay, Robert J.; Zhou, Yalu; Schwartz, Joel L.

doi:10.1111/jop.12523

Cited by 4 publications

(3 citation statements)

References 29 publications

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“…Of the genes coding matrix metallopeptidases, differential expression of MMP11 was found as an early event in oral tumor progression 50 , but that of MMP12 could not be associated with oral cancer progression from previous studies. An immunohistochemical analysis of KRT13 had shown a loss of expression in OSCC cells while it was expressed in normal differentiated basal and suprabasal oral mucosa epithelial cells 51 . Thus, KRT13 can also be treated as a biomarker for progression to OSCC-GB.…”

Section: Discussionmentioning

confidence: 99%

Genes and pathways monotonically dysregulated during progression from normal through leukoplakia to gingivo-buccal oral cancer

et al. 2021

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Oral squamous cell carcinoma of the gingivo-buccal region (OSCC-GB) accounts for the highest cancer morbidity and mortality among men in India. It has been observed that about one-third of individuals with oral leukoplakia, a dysplastic precancerous lesion in the oral cavity, progress to oral cancer. We aimed to identify systematic transcriptomic changes as a normal tissue in the oral cavity progresses to frank OSCC-GB. Seventy-two OSCC-GB patients, from multiple hospitals, were recruited, and transcriptome analysis of tumor and adjacent normal tissue (of all patients) and adjacent leukoplakia tissue (of a subset of 25 unselected patients with concomitant leukoplakia) was performed. We have identified many differences in the transcriptomic profiles between OSCC-GB and squamous cell carcinoma of the head and neck regions. Compared to the normal/precancerous tissue, significant enrichment of ECM−receptor interaction, PI3K-Akt signaling, cytokine−cytokine receptor interaction, focal adhesion, and cell cycle pathways were observed in OSCC-GB. Using gene set enrichment analysis, we identified a profound role of interferon receptor signaling in tumor growth by activating immune evasion mechanisms. The role of tumor-infiltrating immune cells further supported the growth and immunosuppressive mechanism of tumor tissues. Some immune evasion genes—CD274, CD80, and IDO1—were found to be activated even in the precancerous tissue. Taken together, our findings provide a clear insight into the sequential genetic dysregulation associated with progression to oral cancer. This insight provides a window to the development of predictive biomarkers and therapeutic targets for gingivo-buccal oral cancer.

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Section: Discussionmentioning

confidence: 99%

Genes and pathways monotonically dysregulated during progression from normal through leukoplakia to gingivo-buccal oral cancer

et al. 2021

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“…PFN1 has been found to be downregulated in multiple late-stage cancers, including breast, pancreatic, and bladder malignancies . Loss of PFN1 has been preliminarily associated with lymph node metastasis and poorer prognosis in oral cavity cancers, , suggestive of PFN2 as a tumor suppressor, but no association with OPSCC has been identified.…”

Section: Discussionmentioning

confidence: 99%

Comparative Proteomic Analysis of HPV(+) Oropharyngeal Squamous Cell Carcinoma Recurrence

Robinson

Shon

et al. 2021

J. Proteome Res.

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Deintensification therapy for human papillomavirus-related oropharyngeal squamous cell carcinoma (HPV(+) OPSCC) is under active investigation. An adaptive treatment approach based on molecular stratification could identify high-risk patients predisposed to recurrence and better select for appropriate treatment regimens. Collectively, 40 HPV(+) OPSCC FFPE samples (20 diseasefree, 20 recurrent) were surveyed using mass spectrometry-based proteomic analysis via data-independent acquisition to obtain fold change and false discovery differences. Ten-year overall survival was 100.0 and 27.7% for HPV(+) disease-free and recurrent cohorts, respectively. Of 1414 quantified proteins, 77 demonstrated significant differential expression. Top enriched functional pathways included those involved in programmed cell death (73 proteins, p = 7.43 × 10 −30 ), apoptosis (73 proteins, p = 5.56 × 10 −9 ), β-catenin independent WNT signaling (47 proteins, p = 1.45 × 10 −15 ), and Rho GTPase signaling (69 proteins, p = 1.09 × 10 −5 ). PFN1 (p = 1.0 × 10 −3 ), RAD23B (p = 2.9 × 10 −4 ), LDHB (p = 1.0 × 10 −3 ), and HINT1 (p = 3.8 × 10 −3 ) pathways were significantly downregulated in the recurrent cohort. On functional validation via immunohistochemistry (IHC) staining, 46.9% (PFN1), 71.9% (RAD23B), 59.4% (LDHB), and 84.4% (HINT1) of cases were corroborated with mass spectrometry findings. Development of a multilateral molecular signature incorporating these targets may characterize high-risk disease, predict treatment response, and augment current management paradigms in head and neck cancer.

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“…In head and neck squamous cell carcinoma (HNSCC), downregulation of PFN2 reduced phosphorylation/expression of AKT, GSK-3β, and β-catenin, leading to reduced invasion and metastasis [24]. In oral squamous cell carcinoma (OSCC) tissues, PFN1 levels were lower in tumor epithelium and has been associated with lymph node metastasis [25]. In hepatocellular carcinoma profilin was a direct target for miR-19a-3p and low expression of profilin was correlated with poor prognosis in patients [26].…”

Section: Profilin In Cancermentioning

confidence: 99%

Cytoskeletal Remodeling in Cancer

Aseervatham

2020

Biology

101

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Successful metastasis depends on cell invasion, migration, host immune escape, extravasation, and angiogenesis. The process of cell invasion and migration relies on the dynamic changes taking place in the cytoskeletal components; actin, tubulin and intermediate filaments. This is possible due to the plasticity of the cytoskeleton and coordinated action of all the three, is crucial for the process of metastasis from the primary site. Changes in cellular architecture by internal clues will affect the cell functions leading to the formation of different protrusions like lamellipodia, filopodia, and invadopodia that help in cell migration eventually leading to metastasis, which is life threatening than the formation of neoplasms. Understanding the signaling mechanisms involved, will give a better insight of the changes during metastasis, which will eventually help targeting proteins for treatment resulting in reduced mortality and longer survival.

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A loss of profilin‐1 in late‐stage oral squamous cell carcinoma

Cited by 4 publications

References 29 publications

Genes and pathways monotonically dysregulated during progression from normal through leukoplakia to gingivo-buccal oral cancer

Genes and pathways monotonically dysregulated during progression from normal through leukoplakia to gingivo-buccal oral cancer

Comparative Proteomic Analysis of HPV(+) Oropharyngeal Squamous Cell Carcinoma Recurrence

Cytoskeletal Remodeling in Cancer

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