Changed Expression of E-cadherin and Galectin-9 in Oral Squamous Cell Carcinomas but Lack of Potential as Prognostic Markers

Sp, Chan; Kallarakkal, Thomas George; Abraham, Mannil Thomas

doi:10.7314/apjcp.2014.15.5.2145

Cited by 20 publications

(16 citation statements)

References 44 publications

(84 reference statements)

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“…B7‐H4 and Galectin‐9, two recognized inhibitory immune checkpoints, play significant roles in tumorigenesis. Both have been found to be upregulated in OSCC . In the present study, we also found that expression of INPP4B was positively correlated with expression of B7‐H4 and Galectin‐9.…”

Section: Discussionsupporting

confidence: 83%

Expression of inositol polyphosphate 4‐phosphatase type II and the prognosis of oral squamous cell carcinoma

Yang

Xiao

et al. 2020

European J Oral Sciences

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Inositol polyphosphate 4‐phosphatase type II (INPP4B) is a phosphoinositide phosphatase that plays complex roles in the pathogenesis of different tumors. We aimed to explore the expression, clinicopathological significance, and prognostic value of INPP4B in oral squamous cell carcinoma (OSCC). Tissue microarrays that included samples from 176 primary OSCCs, 42 normal mucosae, and 69 dysplastic tissues were used for immunostaining analyses of INPP4B protein. Aperio ScanScope CS scanner and aperio quantification software were used to scan the microarrays and score the staining, respectively. We also evaluated the correlation between INPP4B expression and clinical parameters, pathological grades, node‐positive status, and immune‐related markers. Expression of INPP4B was statistically significantly upregulated in human primary OSCC tissues compared with dysplastic and normal tissues. Additionally, we found that patients with strong expression of INPP4B had a statistically significantly poorer overall survival than patients with weak expression of INPP4B. Furthermore, our study indicated that expression of INPP4B in OSCC was positively associated with expression of p‐S6Ser235/236, p‐CADSer1859, and certain immune checkpoints (B7‐H4, Galectin‐9). Therefore, INPP4B may be an independent prognostic indicator for patients with OSCC, in which it might function as an oncoprotein.

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Section: Discussionsupporting

confidence: 83%

Expression of inositol polyphosphate 4‐phosphatase type II and the prognosis of oral squamous cell carcinoma

Yang

Xiao

et al. 2020

European J Oral Sciences

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“…Our results also show that in a high percentage of samples from OCSCC N + , loss of E-cadherin expression in the membrane was associated with the cytoplasmic and nuclear expression of this protein by neoplastic cells. While other authors have also shown similar results [ 16 , 25 ], the intensity and frequency of the cytoplasmic expression of E-cadherin by neoplastic cells remains controversial [ 23 , 28 ]. Therefore, additional studies are needed in order to clarify the mechanisms by which the reduction and loss of E-cadherin expression during malignant transformation occurs.…”

Section: Discussionmentioning

confidence: 77%

E-cadherin as a potential biomarker of malignant transformation in oral leukoplakia: a retrospective cohort study

et al. 2014

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BackgroundNumerous attempts have been made to establish and develop tumor markers that could determine the susceptibility of normal tissues to transform into cancerous ones. To determine whether altered expression patterns of E-cadherin could be an early event in the progression of potentially malignant disorders to oral squamous cell carcinoma, this study aimed to assess the relationship between the immunoexpression of E-cadherin and the different degrees of epithelial dysplasia in oral leukoplakia.MethodsSurgically excised specimens from patients with oral leukoplakia (n = 31), oral cavity squamous cell carcinoma with cervical lymph node metastasis (n = 12) and normal oral mucosa (n = 9) were immunostained for E-cadherin. Oral leukoplakia samples were distributed into low and high risk group according to a binary system for grading oral epithelial dysplasia. Comparative analyses between E-cadherin expression and microscopic features (WHO histological grading and epithelial dysplasia) were performed by Pearson Chi-square test (P < 0.05).ResultsDifferences in E-cadherin expression were observed between normal oral mucosa and low risk oral leukoplakia (P = 0.006), low and high risk oral leukoplakia (P = 0.019), and high risk oral leukoplakia and oral cavity squamous cell carcinoma with cervical lymph node metastasis (P = 0.0001). In addition, as epithelia undergo dysplastic changes, the risk of malignant transformation increases, and there is a reduction or loss of E-cadherin expression by keratinocytes. Reduced E-cadherin expression was an early phenomenon and it was observed in moderate-severe dysplasia, showing that the loss of epithelial cohesion may be an indicator of progression to oral cavity squamous cell carcinoma.ConclusionsE-cadherin could be used as a novel biomarker to identify lesions with potential risk for malignant transformation, which may provide opportunities for prophylactic interventions in high risk patient groups.

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“…In addition, the E-cadherin protein was found to be downregulated, whereas fibronectin was upregulated following infection of the KLF cDNA vector (20). Findings of recent studies have shown that the epithelial cell adhesion molecule E-cadherin is often downregulated during carcinoma progression and metastatic tumor spread (21)(22)(23)(24). These observations suggest that KLF8 plays a vital role in EMT in gastric cancer cells.…”

Section: Discussionmentioning

confidence: 95%

Krüppel-like factor 8 involved in hypoxia promotes the invasion and metastasis of gastric cancer via epithelial to mesenchymal transition

Liu¹,

Wang²,

Zhou³

et al. 2014

Oncology Reports

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Abstract. Previously, we reported that hypoxia was able to induce invasion and metastasis in gastric cancer and that hypoxia-inducible factor-1 (HIF-1) is a key factor involved in this tumor type. Krüppel-like factor 8 (KLF8) as a transcriptional repressor has been suggested as a promoter of tumor metastasis in breast cancer and an inducer of the epithelial-mesenchymal transition (EMT). KLF8 is also highly expressed in gastric cancer tissues, contributing to poor prognosis. However, the association between KLF8 and HIF-1 in regulating the progression of human gastric cancer in hypoxia is unclear. In the present study, we found that KLF8 was overexpressed in gastric cancer metastatic tissues and cells. Additionally, KLF8 siRNA significantly inhibited SGC7901 cell invasion and migration compared with SGC7901, SGC7901/Scr-si cells. Hypoxia is thus able to induce KLF8 expression and EMT in SGC7901 cells. However, following the examination of changes in cell morphology and epithelial and mesenchymal markers, it was found that KLF8 siRNA and HIF-1 siRNA strongly reversed EMT in cells undergoing hypoxia. Furthermore, hypoxia-induced KLF8 overexpression was attenuated by HIF-1 siRNA. Experiments using luciferase promoter constructs resulted in a marked increase in the activity of cells exposed to hypoxia and decreased activity in cells co-transfected with HIF-1 siRNA. The chromatin immunoprecipitation assay revealed proximal HRE at -133 is the main HIF-1 binding site in the KLF8 promoter.In conclusion, the results demonstrated that KLF8 is actively enhanced by hypoxia and is a novel HIF-1 target. KLF8 is a novel EMT regulating transcription factor that involved in the progression of gastric cancer. The specific anti-EMT drugs in combination with anti-hypoxia are new promising cancer therapies.

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Changed Expression of E-cadherin and Galectin-9 in Oral Squamous Cell Carcinomas but Lack of Potential as Prognostic Markers

Cited by 20 publications

References 44 publications

Expression of inositol polyphosphate 4‐phosphatase type II and the prognosis of oral squamous cell carcinoma

Expression of inositol polyphosphate 4‐phosphatase type II and the prognosis of oral squamous cell carcinoma

E-cadherin as a potential biomarker of malignant transformation in oral leukoplakia: a retrospective cohort study

Krüppel-like factor 8 involved in hypoxia promotes the invasion and metastasis of gastric cancer via epithelial to mesenchymal transition

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