Browsing by Subject "Oral squamous cell carcinoma"

Now showing 1 - 7 of 7
  • Thumbnail Image
    Publication
    Open Access
    Expression of basal cell keratin 15 and keratin 19 in oral squamous neoplasms represents diverse pathophysiologies
    (F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2012) Khanom, Rumana; Sakamoto, Kei; Kumar Pal, Samir; Shimada, Yasuyuki; Morita, Kei-ichi; Omura, Ken; Miki, Yoshio; Yamaguchi, Akira
    Human epithelium contains keratin, which is expressed during differentiation. Depending on the target cell type, different types of keratin are expressed, and their alterations seem to represent changes in cell properties. The basal cells of oral epithelium express keratin 5 (K5), K14, K15 and K19, but their alterations in tumors are unclear. To address this issue and to seek possible diagnostic application, we examined the expression of these keratins in oral squamous cell carcinoma (OSCC) and squamous intraepithelial neoplasm (SIN). cDNA microarray analysis of 43 OSCC revealed slight upregulation of KRT14, downregulation of KRT15 and KRT19, and unaltered KRT5 expression. There were great variations in KRT15 and KRT19 expression across each cancer. Well-differentiated OSCC tended to express more KRT15 and less KRT19 compared to moderately- or poorly-differentiated OSCC. KRT15 was positively correlated with differentiation-related keratin, KRT13. These observations were further investigated by immunohistochemical examination. K5 and K14 were ubiquitously expressed in all 50 OSCC and 50 SIN examined. K15 and K19 were generally downregulated, but were considerably retained in about half of the cases and showed diverse expression patterns. K15-positive cancers tended to show a well-differentiated phenotype, and K19-positive cancers tended to show more invasive tumor fronts. Most K19-positive cancers appeared to develop with little associating SIN. K19 was consistently downregulated in SIN, while K15 was downregulated mainly in high grade SIN. In summary, K15 and K19, unlike K5 or K14, are expressed variably in both SIN and OSCC, which reflects the differences in their pathogenesis and biological behaviors, suggesting their prospective applications as markers for subclassifying OSCC and SIN
  • Thumbnail Image
    Publication
    Open Access
    Localization of Fusobacterium nucleatum in oral squamous cell carcinoma and its possible directly interacting protein molecules: A case series
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2023) He, Xuan; Ma, Xuemeng; Meng, Zijun; Han, Zhiqi; Chen, Wenxia
    Introduction. While 15 to 20% of cancers are associated with microbial infection, the relationship between oral microorganisms and oral squamous cell carcinoma (OSCC) remains unclear. The location of bacteria in a tumor is closely related to its carcinogenic mechanism. The aim of this study was to analyse bacterial diversity in clinical OSCC tissue samples and tumor distant normal tissues, locate target bacteria, and search for proteins that may interact with target bacteria. Materials and Methods. The 16S rDNA method was used to analyse bacterial diversity in clinical OSCC tissue samples and tumor distant normal tissues. Correlations between Fusobacterium abundance and clinicopathological characteristics were analysed using the χ2 test. The position of target bacteria was analysed by fluorescence in situ hybridization (FISH), and the expression of CK, CD31, CD45, CD68, cyclin D1, βcatenin, E-cadherin, NF-κB, and HIF-1α was analysed by immunohistochemistry (IHC) in OSCC tumor tissues and tumor distant normal tissues. Results. The 16S rDNA results showed that the detected amount of Fusobacterium in OSCC tumor tissues was significantly larger than that in tumor distant normal tissues. High expression of Fusobacterium was significantly correlated with the lifestyle-related oral risk habits, including smoking (p=0.036) and alcohol consumption (p=0.022), but did not correlate with patient sex, age, tumor laterality, tumor size, grade or TNM stage. Fusobacterium nucleatum was enriched in tumor stroma, where CD31+ blood vessels and inflammatory cells (including CD45+ leukocytes and CD68+ macrophages) were densely distributed. Cyclin D1 was mainly expressed in the nucleus of tumor cells. β-catenin was expressed in the tumor cell membrane and was positively expressed in tumor interstitial vascular endothelial cells. E-cadherin was mainly expressed in tumor cell membranes. NF-κB was positively expressed in the cytoplasm of tumor cells, tumor interstitial cells and myo-fibrocytes. HIF-1α was mainly expressed in the cytoplasm of tumor interstitial cells. HIF-1α was highly expressed where Fusobacterium nucleatum was densely distributed. Conclusion. According to our study, the detected amount of Fusobacterium in OSCC tumor tissues was significantly larger than that in tumor distant normal tissues, and Fusobacterium nucleatum might aggravate inflammation and hypoxia by interacting with NF-κB and HIF-1α in OSCC.
  • Thumbnail Image
    Publication
    Open Access
    MiR-503-5p functions as an oncogene in oral squamous cell carcinoma by targeting Smad7
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Fei, Yifan; Shan, Weilan; Chen, Xiaoqing
    Background. Oral squamous cell carcinoma (OSCC) is a common oral malignancy. Previous studies indicated that the level of miR-503-5p was upregulated in OSCC tissues. However, the mechanism by which miR-503-5p regulates the proliferation and invasion of OSCC cells remains unclear. Therefore, this study aimed to investigate the role of miR-503-5p during the progression of OSCC. Methods. The level of miR-503- 5p in Tca8113 cells was detected using RT-qPCR assay. In addition, CCK-8, transwell assays and flow cytometry assays were conducted to detect cell viability, migration, invasion and apoptosis, respectively. Meanwhile, the dual luciferase reporter assay was applied to explore the interaction between miR-503-5p and Smad7 in Tca8113 cells. Results. Overexpression of miR-503-5p significantly promoted the proliferation, migration and invasion of Tca8113 cells, while downregulation of miR- 503-5p markedly inhibited proliferation, migration and invasion of cells. In addition, knockdown of miR-503-5p obviously induced the apoptosis of Tca8113 cells via increasing the levels of Bax and cleaved caspase 3, and decreased the expression of Bcl-2. Moreover, SMAD family member 7 (Smad7) was identified as a direct binding target of miR-503-5p in Tca8113 cells. Overexpression of miR-503-5p significantly downregulated the levels of Smad7 and E-cadherin, but upregulated the levels of N-cadherin and MMP-9 in Tca8113 cells. Conclusion. These results indicated that miR-503-5p might act as an oncogene in OSCC cells by targeting Smad7. Therefore, miR-503-5p might act as a novel and potential therapeutic target for the treatment of OSCC
  • Thumbnail Image
    Publication
    Open Access
    MiR-590-5p regulates cell proliferation, apoptosis, migration and invasion in oral squamous cell carcinoma by targeting RECK
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Bao, Wei-Wei; Shi, You-Ling; Ma, Yan; Qu, Xing-Hui; Pang, Guang-Ming; Yang, Lei
    Objective. To discover the role of miR-590- 5p in oral squamous cell carcinoma (OSCC) progression and the corresponding mechanism via the targeting RECK. Methods. OSCC (n=85) and normal oral tissues (n=60) were collected to quantify the miR-590-5p expression by using qRT-PCR. Then SCC-15 and OECM1 cells were selected and divided into Mock, inhibitor NC, miR-590-5p inhibitor, si-RECK and miR-590-5p inhibitor + si-RECK groups. Dual-luciferase reporter gene assay was used to verify if miR-590-5p could target RECK. The biological behaviors of OSCC cells were evaluated by MTT, Wound-healing, Transwell and Flow cytometry. The expression of miR-590-5p and RECK was measured by qRT-PCR and Western blotting, respectively. Results. Overexpression of miR-590-5p was found in OSCC tissues. The expression of miR-590-5p was significantly associated with the clinical TNM stage, differentiation degree, and lymph node metastasis of OSCC. RECK was identified as a direct target of miR590-5p. Compared with the Mock group, cells in the miR-590-5p inhibitor group were decreased in terms of proliferation, invasion, and migration, and increased in cell apoptosis, accompanied by down-regulated miR590-5p, Bcl-2/Bax and MMP-9, and up-regulated RECK. By contrast, si-RECK group presented completely opposite changes, and si-RECK reversed the inhibitory effect of miR-590-5p inhibitor on the OSCC cell growth. Conclusion. MiR-590-5p expression was obviously increased in OSCC, and inhibiting miR-590-5p enhanced the expression of its target gene RECK, thereby suppressing proliferation, migration and invasion of OSCC cells and promoting apoptosis of OSCC cells
  • Thumbnail Image
    Publication
    Open Access
    Notch1 in oral squamous cell carcinoma
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Yoshida, Ryoji; Ito, Takaaki; Abdo Hassan, Wael; Nakayama, Hideki
    Notch signaling has been reported to be involved in several types of malignant tumors. However, the role and activation mechanisms of Notch signaling in oral squamous cell carcinoma (OSCC) remain poorly characterized. The present review focuses on the dual role of Notch signaling in OSCC. A number of expression and functional analyses demonstrated that Notch1 plays a crucial role in development and progression of OSCC. On the other hand, a tumor suppressive role of Notch1 was also suggested from studies, based on deep sequencing of cancer genomes. Interestingly, although some Notch1 mutations overlap in tumors from Caucasian and Asian patients, the overall spectrum of such mutations is vastly different between these cohorts. Accumulating evidence suggests that variation of Notch1 mutation signature may determine the role of Notch signaling in OSCC. As Notch is thought to act as an oncogene in a subset of OSCC, but also has a tumor suppression role, the role of Notch in OSCC seems to be highly context dependent.
  • Thumbnail Image
    Publication
    Open Access
    Tumour-associated tissue eosinophilia (TATE) in oral squamous cell carcinoma: a comprehensive review
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Mascitti, Marco; Togni, Lucrezia; Rubini, Corrado; Troiano, Giuseppe; Muzio, Lorenzo Lo; Santarelli, Andrea
    Oral squamous cell carcinoma is the most common head and neck malignancy, characterised by high invasive capacity, lymph node metastasis, and high recurrence rate. Among the morphological features of oral cancer, the tumour-associated tissue eosinophilia has gained growing interest in the last years. Eosinophils are a minor subpopulation of leukocytes, representing 1- 3% of all circulating white blood cells. The presence of high levels of eosinophils is associated with several diseases, but their role in cancer pathophysiology is controversial. In particular, an uncertain and contradictory relationship exists between the exact role of tumour-associated tissue eosinophilia and oral cancer development. Many studies have shown that tumour- associated tissue eosinophilia increases both in the progression of oral potentially malignant disorders as well as in the grade and stage progression of oral cancer. Despite this, both negative and positive prognostic outcomes have been associated with eosinophil infiltration. The heterogeneous results may be partially due both to several methodological inconsistencies and to an incorrect interpretation of the physiological role of eosinophils. Therefore, further studies to elucidate the contribution of eosinophil infiltration are needed, focusing on the existence of eosinophil subpopulations regulated by the cancer immune microenvironment. Furthermore, the correct reporting of prognostic marker research is encouraged, in order to ensure the reproducibility and the comparability of the results from different studies
  • Thumbnail Image
    Publication
    Open Access
    Upregulation of LY6K induced by FTO-mediated demethylation promotes the tumorigenesis and metastasis of oral squamous cell carcinoma via CAV-1-mediated ERK1/2 signaling activation
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2024) Xu, Chen; Gong, Rujuan; Yang, Haibing
    Lymphocyte antigen 6 complex locus K (LY6K) has been demonstrated to play a significant role in cancers and identified as a therapeutic biomarker for head and neck squamous cell carcinoma. However, the role of LY6K in oral squamous cell carcinoma (OSCC) has not been explored. The current study discovered that LY6K was aberrantly upregulated in OSCC cell lines and tissues and that high LY6K expression significantly correlated with poorer survival of OSCC patients. Through stable knockdown of LY6K, we found that the growth, colony formation, migration, and invasion of OSCC cells were substantially suppressed. In addition, tumor growth and lung metastasis in vivo were effectively inhibited by LY6K depletion. Mechanically, LY6K binds with CAV-1 and activates CAV-1-mediated MAPK/ERK signaling to exert its oncogenic effects on OSCC. In addition, LY6K expression in OSCC was discovered to be regulated by FTO-mediated RNA N6- methyladenosine (m6A) modification in an IGF2BP1- dependent manner. Generally, LY6K expression was upregulated by FTO-mediated demethylation in OSCC, which promoted the tumorigenesis and metastasis of OSCC via activating the CAV-1-mediated ERK1/2 signaling pathway