Epithelial–Mesenchymal Transition Predicts Survival in Oral Squamous Cell Carcinoma

Wangmo, Chimi; Charoen, Nattinee; Jantharapattana, Kitti; Dechaphunkul, Arunee; Thongsuksai, Paramee

doi:10.1007/s12253-019-00731-z

Cited by 28 publications

(28 citation statements)

References 26 publications

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“…Thus, the extracellular acidification might be another driving force to adapt the E-cadherin/vimentin balance. A loss of E-cadherin in combination with an overexpression of vimentin are early steps in the EMT cascade [ 68 ]. The acidification of the extracellular matrix and the maintenance of an optimal pH for sustaining cancer growth has been well investigated.…”

Section: Hif-1α Stabilization Under Normoxia Its Role In Glutaminmentioning

confidence: 99%

Current Understanding of the HIF-1-Dependent Metabolism in Oral Squamous Cell Carcinoma

Eckert

Kappler

Große

et al. 2020

IJMS

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Oral squamous cell carcinoma (OSCC) is the 10th most frequent human malignancy and is thus a global burden. Despite some progress in diagnosis and therapy, patients’ overall survival rate, between 40 and 55%, has stagnated over the last four decades. Since the tumor node metastasis (TNM) system is not precise enough to predict the disease outcome, additive factors for diagnosis, prognosis, prediction and therapy resistance are urgently needed for OSCC. One promising candidate is the hypoxia inducible factor-1 (HIF-1), which functions as an early regulator of tumor aggressiveness and is a key promoter of energy adaptation. Other parameters comprise the composition of the tumor microenvironment, which determines the availability of nutrients and oxygen. In our opinion, these general processes are linked in the pathogenesis of OSCC. Based on this assumption, the review will summarize the major features of the HIF system-induced activities, its target proteins and related pathways of nutrient utilization and metabolism that are essential for the initiation, progression and therapeutic stratification of OSCC.

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Section: Hif-1α Stabilization Under Normoxia Its Role In Glutaminmentioning

confidence: 99%

Current Understanding of the HIF-1-Dependent Metabolism in Oral Squamous Cell Carcinoma

Eckert

Kappler

Große

et al. 2020

IJMS

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“…The OVMANA, SMOV-2 TU-OC-I, RMG-I, and OVSAYO lines displayed a distinctly epithelial phenotype. The loss of E-cadherin and concomitant gain of vimentin expression is indicative of cells having undergone an epithelial to mesenchymal transition, which is often associated with more aggressive forms of cancer [50][51][52][53]. It is also notable that the expression of these phenotypic markers does not correlate with a distinct gene mutational profile in OCCC cell lines, the morphology of the spheroids they generate in suspension culture or whether the cell line proliferates in suspension culture.…”

Section: Genetic and Molecular Characterizationmentioning

confidence: 99%

Characterization of Mutational Status, Spheroid Formation, and Drug Response of a New Genomically-Stable Human Ovarian Clear Cell Carcinoma Cell Line, 105C

Kolendowski

Valdes

Hirte

et al. 2020

Cells

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Ovarian clear cell carcinoma (OCCC) is a rare subtype of gynecological cancer for which well-characterized and authenticated model systems are scarce. We provide an extensive characterization of ‘105C’, a cell line generated from an adenocarcinoma of the clear cell histotype using targeted next-generation sequencing, cytogenetic microarrays, along with analyses of AKT/mTOR signaling. We report that that the 105C cell line is a bona fide OCCC cell line, carrying PIK3CA, PTEN, and ARID1A gene mutations, consistent with OCCC, yet maintain a stable genome as reflected by low copy number variation. Unlike KOC-7c, TOV-21G, and RMG-V OCCC lines also mutated for the above genes, the 105C cells do not carry mutations in mismatch repair genes. Importantly, we show that 105C cells exhibit greater resistance to mTOR inhibition and carboplatin treatment compared to 9 other OCCC cell lines in 3D spheroid cultures. This resistance may be attributed to 105C cells remaining dormant in suspension culture which surprisingly, contrasts with several other OCCC lines which continue to proliferate in long-term suspension culture. 105C cells survive xenotransplantation but do not proliferate and metastasize. Collectively, we show that the 105C OCCC cell line exhibits unique properties useful for the pre-clinical investigation of OCCC pathobiology.

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“…Oral squamous cell carcinoma (OSCC) is a malignant epithelial cancer that threatens the health of individuals worldwide and OSCC frequently occurs in the tongue and buccal mucosa ( 1 – 3 ). The 5-year survival for human OSCC patients is approximately 50% and the incidence of OSCC is still increasing with a reported annual incidence worldwide of approximately 275,000 ( 4 , 5 ) and 50,000 in China ( 6 ).…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA PVT1 promotes tumor cell proliferation, invasion, migration and inhibits apoptosis in oral squamous cell carcinoma by regulating miR‑150‑5p/GLUT‑1

Ren

2020

Oncol Rep

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Oral squamous cell carcinoma (OSCC) is a cancer with high morbidity and mortality. Research has demonstrated that long non-coding RNAs (lncRNAs) are critical for tumor initiation and development. In the present study, we aimed to ascertain the functions and potential mechanisms of lncRNA plasmacytoma variant translocation 1 (PVT1) in OSCC. Firstly, we found that the expression of PVT1 was increased in human OSCC tumor tissues and it was related to reduced survival of the patients. Furthermore, miR-150-5p expression was downregulated in OSCC tumor tissues and it was negatively related with PVT1. Moreover, GLUT-1 protein expression was upregulated in human OSCC tumor tissues. In addition, cell proliferation capacity was measured by CCK-8 assay and cell invasion and migration were measured by Transwell assay. PVT1 overexpression promoted cell proliferation, invasion and migration, while these effects were abrogated by PVT1 downregulation. In addition, luciferase gene reporter assay verified the miR-150-5p directly binds with PVT1, which regulates the biological functions of OSCC. Additionally, luciferase gene reporter assay confirmed that GLUT-1 was a target for miR-150-5p. The promotion of cell proliferation, invasion and migration in LV-PVT1-transfected cells was eliminated following miR-150-5p overexpression. Finally, in vivo nude mouse xenograft model further verified that PVT1 knockdown inhibited tumor growth, formation, invasion and migration. According to the results, PVT1 is increased in human OSCC tumor tissues, and is related to the poor prognosis of human OSCC patients. We uncovered a previously unappreciated PVT1/miR-150-5p/GLUT-1 signaling axis that promotes cell proliferation, invasion, migration and inhibits apoptosis in OSCC cell lines and in vivo , which suggests that this axis could be a target for the treatment of OSCC.

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Epithelial–Mesenchymal Transition Predicts Survival in Oral Squamous Cell Carcinoma

Cited by 28 publications

References 26 publications

Current Understanding of the HIF-1-Dependent Metabolism in Oral Squamous Cell Carcinoma

Current Understanding of the HIF-1-Dependent Metabolism in Oral Squamous Cell Carcinoma

Characterization of Mutational Status, Spheroid Formation, and Drug Response of a New Genomically-Stable Human Ovarian Clear Cell Carcinoma Cell Line, 105C

Long noncoding RNA PVT1 promotes tumor cell proliferation, invasion, migration and inhibits apoptosis in oral squamous cell carcinoma by regulating miR‑150‑5p/GLUT‑1

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