scholarly journals Spontaneous emergence of non-convertible cell states with CD24-High phenotype results in phenotypic heterogeneity that associates with poor prognosis in oral cancer

2021 ◽  
Author(s):  
Kavya Vipparthi ◽  
Kishore Hari ◽  
Priyanka Chakraborty ◽  
Subhashis Ghosh ◽  
Ankit Kumar Patel ◽  
...  
Keyword(s):  
Population Dynamics ◽  
Oral Cancer ◽  
Cancer Cells ◽  
Aldh Activity ◽  
Induced Stress ◽  
Response To Chemotherapy ◽  
Oral Tumors ◽  
Alternate States ◽  
Oral Cancer Cells

AbstractCancer cells within individual tumors often exist in distinct phenotypic states contributing to intratumoral heterogeneity (ITH). However, studies on cell state dynamics among oral cancer cells are largely missing. Here, we have multiplexed phenotypic markers of putative oral-stem-like cancer cells (SLCCs) and characterized diversity among CD44-positive oral cancer cell subpopulations with respect to distinct expression of CD24 and aldehyde dehydrogenase (ALDH)-activity. Our in vitro experimental observations were explained by a Markov model where subpopulations followed two distinct patterns of spontaneous repopulation dynamics. Cells showed stochastic inter-conversions on ALDH-axis, harnessed by cancer cells to enrich ALDHHigh subpopulations in response to Cisplatin treatment. However, these cells followed a strict non-interconvertible transition of CD24Low to CD24High subpopulations, even in response to chemotherapy-induced stress. Using phenotype-specific RNAseq, we suggest the organization of subpopulations into hierarchical structure with possible maintenance of intermediate alternate states of stemness within the differentiating oral cancer cells. We also show that the population dynamics described here may influence tumor behaviour by increasing ITH in aggressive oral tumors. Overall, the described phenotypic subgroups not only reliably exhibited spontaneous or Cisplatin-driven cellular dynamics but also the distinct transcription states of oral cancer cells. Most importantly, our in vitro model system derived observations emphasized the prognostic power which may be translated for betterment of oral cancer patients.Graphical AbstractWe have characterized diversity among CD44-positive oral cancer cells lines with respect to distinct expression of CD24 and ALDH-activity. Cells showed stochastic inter-conversions on ALDH-axis but a strict non-interconvertible transition of CD24Low to CD24High phenotype, even in response to chemotherapy-induced stress. RNAseq study suggested the organization of subpopulations into hierarchical structure with possible maintenance of intermediate alternate states of stemness within the differentiating oral cancer cells. The described population dynamics may influence tumor behaviour by increasing intratumoral heterogeneity in aggressive oral tumors.

Mechanism for bone invasion of oral cancer cells mediated by interleukin‐6 in vitro and in vivo

Cancer ◽  
2000 ◽  
Vol 89 (9) ◽  
pp. 1966-1975 ◽  
Author(s):  
Masato Okamoto ◽  
Kenji Hiura ◽  
Go Ohe ◽  
Yasuo Ohba ◽  
Kunihoro Terai ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cancer Cells ◽  
Interleukin 6 ◽  
Bone Invasion ◽  
Oral Cancer Cells

Kochia scoparia induces apoptosis of oral cancer cells in vitro and in heterotopic tumors

2016 ◽  
Vol 192 ◽  
pp. 431-441 ◽  
Author(s):  
Hye-Yeon Han ◽  
Haeng-Eun Lee ◽  
Hyung Joon Kim ◽  
Seung-Hwa Jeong ◽  
Jung-Hoon Kim ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cancer Cells ◽  
Kochia Scoparia ◽  
Oral Cancer Cells

scholarly journals Activation of iCaspase-9 in Neovessels Inhibits Oral Tumor Progression

2006 ◽  
Vol 85 (5) ◽  
pp. 436-441 ◽  
Author(s):  
M.S. Pinsky ◽  
W. Song ◽  
Z. Dong ◽  
K. Warner ◽  
B. Zeitlin ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Oral Cancer ◽  
Tumor Progression ◽  
Cancer Cells ◽  
Immunodeficient Mice ◽  
Oral Tumor ◽  
Biodegradable Scaffolds ◽  
Oral Tumors ◽  
Oral Cancer Cells

Tumors of the oral cavity are highly vascularized malignancies. Disruption of neovascular networks was shown to limit the access of nutrients and oxygen to tumor cells and inhibit tumor progression. Here, we evaluated the effect of the activation of an artificial death switch (iCaspase-9) expressed in neovascular endothelial cells on the progression of oral tumors. We used biodegradable scaffolds to co-implant human dermal microvascular endothelial cells stably expressing iCaspase-9 (HDMEC-iCasp9) with oral cancer cells expressing luciferase (OSCC3-luc or UM-SCC-17B-luc) in immunodeficient mice. Alternatively, untransduced HDMEC were co-implanted with oral cancer cells, and a transcriptionaly targeted adenovirus (Ad-VEGFR2-iCasp-9) was injected locally to deliver iCaspase-9 to neovascular endothelial cells. In vivo bioluminescence demonstrated that tumor progression was inhibited, and immunohistochemistry showed that microvessel density was decreased, when iCaspase-9 was activated in tumor-associated microvessels. We conclude that activation of iCaspase-9 in neovascular endothelial cells is sufficient to inhibit the progression of xenografted oral tumors.

scholarly journals circVAPA promotes the proliferation, migration and invasion of oral cancer cells through the miR-132/HOXA7 axis

2021 ◽  
Vol 49 (6) ◽  
pp. 030006052110132
Author(s):  
Hao Chen ◽  
Ye Zhang ◽  
Kankui Wu ◽  
Xiaoyong Qiu
Keyword(s):  
Oral Cancer ◽  
Cancer Cells ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Loss Of Function ◽  
Invasion And Migration ◽  
Oral Cancer Cells ◽  
And Migration

Objective To study the relationship between the circular RNA vesicle-associated membrane protein-associated protein A (circVAPA) and the pathogenesis of oral squamous cell carcinoma. Methods The expression of circVAPA was detected by RT-qPCR. In vitro loss-of-function experiments were performed in Cal-27 cells. The malignant phenotype of cells was evaluated by cell counting kit-8, clone formation and transwell assays. Luciferase reporter assays were used to assess the circVAPA/miR-132/homeobox A (HOXA) regulatory axis. Results circVAPA expression was significantly increased in oral cancer tissues and cells. The overall survival and progression-free survival of patients with oral cancer who exhibited high circVAPA expression were significantly shorter compared with those with low expression. circVAPA expression was closely related to tumor size, TNM stage and distant metastasis. circVAPA knockdown reduced the proliferation, invasion and migration of Cal-27 cells. MiR-132 was identified as a target of circVAPA in Cal-27 cells. Cotransfection with si-circVAPA and miR-132 inhibitor reversed the inhibitory effect of circVAPA knockdown on cell malignant phenotypes. HOXA7 was further identified as a downstream target of miR-132. Conclusion circVAPA is highly expressed in oral cancer, and its abnormal expression might affect the proliferation, invasion and migration of oral cancer cells by modulating the miR-132/HOXA7 signaling axis.

scholarly journals Abstract 5139:F. nucleatuminduces invasive phenotypes in oral cancer cells in vitro

2018 ◽  
Author(s):  
Amani Harrandah ◽  
Sasanka S. Chukkapalli ◽  
Ann Progulske-Fox ◽  
William Dunn ◽  
Kesavalu Lakshmyya ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cancer Cells ◽  
Oral Cancer Cells

Sensory acceptable equivalent doses of β-phenylethyl isothiocyanate (PEITC) induce cell cycle arrest and retard the growth of p53 mutated oral cancer in vitro and in vivo

2018 ◽  
Vol 9 (7) ◽  
pp. 3640-3656 ◽  
Author(s):  
Aroonwan Lam-ubol ◽  
Alison Lea Fitzgerald ◽  
Arnat Ritdej ◽  
Tawaree Phonyiam ◽  
Hui Zhang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Oral Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Induce Cell Cycle Arrest ◽  
Cycle Arrest ◽  
Oral Cancer Cells ◽  
Phenylethyl Isothiocyanate

Sensory acceptable doses of PEITC are selectively toxic to oral cancer cells via ROS-mediated cell cycle arrest.

scholarly journals Upregulation of LGALS1 is associated with oral cancer metastasis

2018 ◽  
Vol 10 ◽  
pp. 175883591879462 ◽  
Author(s):  
Ji-Min Li ◽  
Chien-Wei Tseng ◽  
Chi-Chen Lin ◽  
Ching-Hsuan Law ◽  
Yu-An Chien ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Cancer Metastasis ◽  
Mapk Pathway ◽  
Cancer Tissue ◽  
Mesenchymal Transition ◽  
Oral Cancer Cells

Background: Oral cancer metastasis is a devastating process that contributes to poor prognosis and high mortality, yet its detailed underlying mechanisms remain unclear. Here, we aimed to evaluate metastasis-specific markers in oral cancer and to provide comprehensive recognition concerning functional roles of the specific target in oral cancer metastasis. Methods: Lectin, galactoside-binding, soluble, 1 (LGALS1) was identified by secretomic analysis. LGALS1 expression of patient samples with oral cancer on the tissue microarray were examined by immunochemical (IHC) staining. Small interfering RNA (siRNA)-mediated knockdown of LGALS1 revealed the role of LGALS1 in oral cancer metastasis in vitro and in vivo. Results: LGALS1 was observed to be upregulated in highly invasive oral cancer cells, and elevated LGALS1 expression was correlated with cancer progression and lymph node metastasis in oral cancer tissue specimens. Functionally, silencing LGALS1 resulted in suppressed cell growth, wound healing, cell migration, and cell invasion in oral cancer cells in vitro. Knockdown of LGALS1 in highly invasive oral cancer cells dramatically inhibited lung metastasis in an in vivo mouse model. Mechanistic studies suggested p38 mitogen-activated protein kinase (MAPK) phosphorylation, upregulated MMP-9, and mesenchymal phenotypes of epithelial-mesenchymal transition (EMT) in highly invasive oral cancer cells, whereas siRNA against LGALS1 resulted in the inactivation of p38 MAPK pathway, downregulated MMP-9, and EMT inhibition. Conclusions: These findings demonstrate that elevated LGALS1 is strongly correlated with oral cancer progression and metastasis, and that it could potentially serve as a prognostic biomarker and an innovative target for oral cancer therapy.

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