Vimentin expression and the influence of Matrigel in cell lines of head and neck squamous cell carcinoma

Vechio, Aluana Maria da Costa Dal; Giudice, Fernanda Salgueiredo; Sperandio, Felipe Fornias; Mantesso, Andréa; Pinto, Décio dos Santos

doi:10.1590/s1806-83242011000300008

Cited by 11 publications

(10 citation statements)

References 22 publications

(25 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We found that all markers were detectable in the 51 malignant PT specimens with the following frequencies among different patients: GD2 (100%, 51/51) CD166 (78.4%, 40/51), CD90 (78.4%, 40/51), CD44 (68.6%, 35/51), CD106 (29.4%, 15/51), CD29 (27.4%, 14/51) and CD105 (1.9%, 1/51) (Table 1). Vimentin was expressed in all tumor specimens, consistent with their mesenchymal lineage [25]. CD117 was expressed in 70.5% of the malignant PT specimens which is in line with the report of its expression in 13% and 67%, of benign and malignant PTs, respectively [26].…”

Section: Resultssupporting

confidence: 75%

Malignant phyllodes tumors display mesenchymal stem cell features and aldehyde dehydrogenase/disialoganglioside identify their tumor stem cells

Lin

Huang

et al. 2014

Breast Cancer Res

View full text Add to dashboard Cite

IntroductionAlthough breast phyllodes tumors are rare, there is no effective therapy other than surgery. Little is known about their tumor biology. A malignant phyllodes tumor contains heterologous stromal elements, and can transform into rhabdomyosarcoma, liposarcoma and osteosarcoma. These versatile properties prompted us to explore their possible relationship to mesenchymal stem cells (MSCs) and to search for the presence of cancer stem cells (CSCs) in phyllodes tumors.MethodsParaffin sections of malignant phyllodes tumors were examined for various markers by immunohistochemical staining. Xenografts of human primary phyllodes tumors were established by injecting freshly isolated tumor cells into the mammary fat pad of non-obese diabetic-severe combined immunodeficient (NOD-SCID) mice. To search for CSCs, xenografted tumor cells were sorted into various subpopulations by flow cytometry and examined for their in vitro mammosphere forming capacity, in vivo tumorigenicity in NOD-SCID mice and their ability to undergo differentiation.ResultsImmunohistochemical analysis revealed the expression of the following 10 markers: CD44, CD29, CD106, CD166, CD105, CD90, disialoganglioside (GD2), CD117, Aldehyde dehydrogenase 1 (ALDH), and Oct-4, and 7 clinically relevant markers (CD10, CD34, p53, p63, Ki-67, Bcl-2, vimentin, and Globo H) in all 51 malignant phyllodes tumors examined, albeit to different extents. Four xenografts were successfully established from human primary phyllodes tumors. In vitro, ALDH+ cells sorted from xenografts displayed approximately 10-fold greater mammosphere-forming capacity than ALDH- cells. GD2+ cells showed a 3.9-fold greater capacity than GD2- cells. ALDH+/GD2+cells displayed 12.8-fold greater mammosphere forming ability than ALDH-/GD2- cells. In vivo, the tumor-initiating frequency of ALDH+/GD2+ cells were up to 33-fold higher than that of ALDH+ cells, with as few as 50 ALDH+/GD2+ cells being sufficient for engraftment. Moreover, we provided the first evidence for the induction of ALDH+/GD2+ cells to differentiate into neural cells of various lineages, along with the observation of neural differentiation in clinical specimens and xenografts of malignant phyllodes tumors. ALDH+ or ALDH+/GD2+ cells could also be induced to differentiate into adipocytes, osteocytes or chondrocytes.ConclusionsOur findings revealed that malignant phyllodes tumors possessed many characteristics of MSC, and their CSCs were enriched in ALDH+ and ALDH+/GD2+ subpopulations.

show abstract

Section: Resultssupporting

confidence: 75%

Malignant phyllodes tumors display mesenchymal stem cell features and aldehyde dehydrogenase/disialoganglioside identify their tumor stem cells

Lin

Huang

et al. 2014

Breast Cancer Res

View full text Add to dashboard Cite

show abstract

“…De Araujo et al (1993) demonstrated that the expression of the Vimentin was most marked in oral squamous cell carcinoma with high tumour grade. Also, significant correlation between Vimentin expression and aggressive tumour features, including lymph node involvement, was recently shown by immunophenotypic analysis of the head and neck squamous cell carcinoma (Mandal et al , 2008; Dal Vechio et al , 2011). Our results did not indicate significant association between Vimentin expression and HPV infection.…”

Section: Discussionmentioning

confidence: 86%

Epithelial-mesenchymal transition-like events in vulvar cancer and its relation with HPV

et al. 2013

View full text Add to dashboard Cite

Background:Epithelial-to-mesenchymal transition (EMT) still remains an obscure event in vulvar squamous cell carcinoma (VSCC).Methods:Immunohistochemistry (IHC) expression of E-cadherin, β-catenin, Snail, Slug, Twist and Vimentin was analysed in 87 VSCC, controlled for human papillomavirus (HPV) positivity, considering tumour front and central tumour as different morphological categories from the same tumour.Results:Lower β-catenin and higher Vimentin expression was associated with invasive front when compared with the central tumour (P=0.013 and P⩽0.001, respectively). Higher expression of E-cadherin in central tumour was significantly related to absence of vascular and perineural invasion, lower invasion depth and ⩽2 lymph node involvement. Loss of β-catenin and high Slug, Snail and Twist expression was associated with HPV-negative tumours. Moreover, β-catenin lower expression associated with gain in Slug expression predicts a subgroup with worst outcome (P=0.001). Lower expression of β-catenin in both central tumour and invasive front correlated with lower overall survival (P=0.021 and P=0.011, respectively). Also, multivariate analysis showed that lower β-catenin expression was independently associated with poorer outcome (P=0.044).Conclusion:Human papillomavirus-related tumours show better prognosis and outcome; besides, they do not progress through EMT phenomenon. Immunohistochemical analysis of β-catenin in invasive tumour front is a key issue for establishing prognosis of vulva cancer.

show abstract

“…Vimentin, an intermediate filament protein type, is associated with a high degree of invasiveness (45,46). It is considered that Matrigel can promote cell invasion of head and neck squamous cell carcinoma cells through increasing vimentin expression in vitro (47).…”

Section: Discussionmentioning

confidence: 99%

Effect of the miR‑96‑5p inhibitor and mimic on the migration and invasion of the SW480‑7 colorectal cancer cell line

Yip

Jabar

et al. 2019

Oncol Lett

View full text Add to dashboard Cite

The objectives of the present study were to identify the aberrant expression of microRNA (miRNA) in colorectal carcinoma (CRC) tissues from published miRNA profiling studies and to investigate the effects of the identified miRNA inhibitor and mimic miR-96-5p on CRC cell migration and invasion. The altered expression of the regulators of cytoskeleton mRNA in miR-96-5p inhibitor-transfected cells was determined. The miR-96-5p expression level in five CRC cell lines, HCT11, CaCo2, HT29, SW480 and SW620, and 26 archived paraffin-embedded CRC tissues were also investigated by reverse-transcriptase quantitative polymerase chain reaction (RT-qPCR). Cell viability in response to the miR-96-5p inhibitor and mimic transfections was determined by an MTT assay. A Matrigel invasion assay was conducted to select the invasive subpopulation designated SW480-7, by using the parental cell line SW480. The effects of miR-96-5p mimic-or inhibitor-transfected SW480-7 cells on cell migration and invasion were evaluated using the Transwell and Matrigel assays, and the change in expression of the regulators of cytoskeleton mRNAs was identified by Cytoskeleton Regulators RT 2-Profiler PCR array followed by validation with RT-qPCR. CRC tissues exhibited a significant increase in miR-96-5p expression, compared with their matched normal adjacent tissues, indicating an oncogenic role for miR-96-5p. The results demonstrated that the miR-96-5p inhibitor decreased the migration of SW480-7 cells, but had no effect on invasion. This may be due to the promotion of cell invasion by Matrigel, which counteracts the blockade of cell invasion by the miR-96-5p inhibitor. The miR-96-5p mimic enhanced SW480-7 cell migration and invasion, as expected. It was determined that there was a >2.5 fold increase in the expression of genes involved in cytoskeleton regulation, myosin light chain kinase 2, pleckstrin homology like domain family B member 2, cyclin A1, IQ motif containing GTPase activating protein 2, Brain-specific angiogenesisinhibitor 1-associated protein 2 and microtubule-actin crosslinking factor 1, in miR-96-5p inhibitor-transfected cells, indicating that they are negative regulators of cell migration. In conclusion, the miR-96-5p inhibitor blocked cell migration but not invasion, and the latter may be due to the counteraction of Matrigel, which has been demonstrated to stimulate cell invasion.

show abstract

Vimentin expression and the influence of Matrigel in cell lines of head and neck squamous cell carcinoma

Cited by 11 publications

References 22 publications

Malignant phyllodes tumors display mesenchymal stem cell features and aldehyde dehydrogenase/disialoganglioside identify their tumor stem cells

Malignant phyllodes tumors display mesenchymal stem cell features and aldehyde dehydrogenase/disialoganglioside identify their tumor stem cells

Epithelial-mesenchymal transition-like events in vulvar cancer and its relation with HPV

Effect of the miR‑96‑5p inhibitor and mimic on the migration and invasion of the SW480‑7 colorectal cancer cell line

Contact Info

Product

Resources

About