Expression of Ki-67 and Βeta-Catenin in Pseudoepitheliomatous Hyperplasia and Squamous Cell Carcinoma in Oral Mucosal Biopsies : An Immunohistochemical Study

Ahmad, Bismah; Asif, Muhammad; Ali, Anam; Jamal, Shahid; Khan, Muhammad Zaib; Khadim, Mohammad Tahir

doi:10.31557/apjcp.2020.21.1.157

Cited by 9 publications

(4 citation statements)

References 16 publications

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“…As indicated by our examination and past investigations performed by Raju et al ,[ 22 ] Dragomir et al ,[ 23 ] and Ahmad et al ,[ 24 ] Ki‑67 ends up being helpful in surveying tumor aggressiveness. Increased cellular proliferation is associated with more advanced lesions, and the distribution of proliferating cells in tissues may disclose about the regulatory mechanisms that become dysfunctional through carcinogenesis.…”

Section: Discussionsupporting

confidence: 69%

An immunohistochemical study showing Ki-67 as an analytical marker in oral malignant and premalignant lesions

et al. 2020

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A BSTRACT Introduction: Ki-67 is a nuclear protein. It is a proliferation marker that has an essential function in tumorigenesis due to its positive connection with tumor expansion. Aim: The aim of this study was to evaluate the articulation of Ki‑67 as prognostic marker in various grades of oral epithelial dysplasia (OED) and in oral squamous cell carcinoma (OSCC). Materials and Methods: A total of 100 histologically affirmed samples of normal oral mucosa (NOM), OED, and OSCC were divided into three groups—Group I (10 samples of normal oral mucosa), Group II (45 samples of OED), Group III (45 samples of OSCC). Routine hematoxylin and eosin and immunohistochemical staining with Ki-67 monoclonal antibody were carried out in all the samples. Results: Within Group I, articulation of Ki-67 was constrained to the basal layers. In Group II, cells showing positive expression of Ki-67 were available in the basal, suprabasal, and spinous layers. Cells showing positive expression of Ki-67 among well-differentiated OSCC were presented mainly in the periphery of the tumor nests; in moderately differentiated OSCC, cells were located in both peripheral and part of a center of the tumor nests; and in most cases of poorly differentiated OSCC, cells were diffused. Statistically significant difference in positive expression of Ki-67 was appreciated between three groups. Conclusion: Ki-67 antigen may perhaps be used as a marker for the histological reviewing of OED and OSCC. With the increase in the severity of OED, cells showing positive expression of Ki-67 also increased.

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Section: Discussionsupporting

confidence: 69%

An immunohistochemical study showing Ki-67 as an analytical marker in oral malignant and premalignant lesions

et al. 2020

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“…While surgical and chemotherapy strategies to treat OSCC have improved significantly, the diagnosis and prognosis of OSCC patients require further investigation. Numerous studies have indicated that cancer cell mutations can promote cell proliferation and metastasis in several cancer types, including OSCC [15,16]. Wnt/β-catenin signaling was shown to play a vital role in the tumorigenesis of malignant tumors which promoted an investigation into whether βcatenin was expressed in the nucleus of OSCC cells [6,17].…”

Section: Discussionmentioning

confidence: 99%

Involvement of RUVBL1 in WNT/β-Catenin Signaling in Oral Squamous Cell Carcinoma

et al. 2022

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Oral squamous cell carcinoma (OSCC) is the most common malignant tumor of head and neck squamous cell carcinoma (HNSCC), but the causes and molecular mechanisms remain unclear. The wingless-integrated/β-catenin (WNT/β-catenin) signaling pathway plays a vital role in cancer cell proliferation, differentiation, and metastasis, including OSCC. To screen potential β-catenin-associated genes involved in OSCC, the intersection of these genes in the STRING and IMEx databases was assessed using differential expression genes (DEG) from public microarrays, and 22 were further selected to construct a β-catenin-protein interaction network. The top 14 hub genes (node degree > 10 ) within the network were selected. Pearson’s correlation analysis showed that β-catenin expression correlated positively with the expression of 11 genes, including AR, BIRC5, CDK6, DKK1, GSK3B, MET, MITF, PARD3, RUVBL1, SLC9A3R1, and SMAD7. A heat map of overall hub gene survival was created, and elevated expression of DKK1 and RUVBL1 was associated with poor survival using the Mantel-Cox test. To identify the function of RUVBL1, colony formation assay, transwell assay, and western blotting revealed that knock-down of RUVBL1 by siRNA decreased H157 and Cal-27 cell proliferation and metastasis by inhibiting β-catenin signaling. These findings suggest that RUVBL1 may serve as a diagnostic and prognostic biomarker for OSCC, as well as a therapeutic target, and may help to uncover additional molecular mechanisms of β-catenin-driven OSCC tumorigenesis.

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“…Therefore, it is important to explore the correlation between β-catenin and Notum in OSCC. Studies have shown that β-catenin is expressed in OSCC tissue [30]. However, its mechanism of action is unclear.…”

Section: Discussionmentioning

confidence: 99%

Notum Promotes Proliferation and Migration of Oral Squamous Cell Carcinoma Via Shh/p-GSK3β/β-Catenin Pathway

Yang

Zhou

et al. 2021

Preprint

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Background: Oral squamous cell carcinoma (OSCC) is a common malignant tumor of the head and neck, accounting for more than 90% of oral and maxillofacial malignancies. Therefore, it is of great importance to explore the key factors regulating OSCC. Notum belongs to the α/β hydrolase family and is a deacylated extracellular protein that regulates Wnt and other signaling pathways. Studies have found that Notum participates in the progression of colorectal cancer and hepatocellular carcinoma and targeting Notum can regulate the occurrence of cancer. However, the relationship between Notum and OSCC is currently unclear. This study aims to explore the role of Notum in regulating OSCC and its specific mechanism. Methods: Nine OSCC tissue sections were selected for hematoxylin and eosin staining and immunohistochemistry for PCNA and Notum. Bioinformatics analysis was used to explore the correlation between OSCC and Notum expression. CCK8, Western blot, RT-PCR, scratch experiment, transwell, clone formation, flow cytometry, cellular immunofluorescence and in vivo nude mouse tumor formation methods were applied to OSCC cells treated with Notum human recombinant protein, a Notum overexpression plasmid, and a Notum small interfering RNA to explore the mechanism of Notum in regulating OSCC. Results: The results of immunohistochemistry and bioinformatics analysis showed that Notum was highly expressed in OSCC tissues. Notum human recombinant protein promoted the proliferation and migration of Cal-27 and SCC-15 cells; overexpression of Notum promoted the proliferation and migration of Cal-27 and SCC-15 cells; si-Notum can significantly inhibit proliferation and migration of Cal-27 and SCC-15 cells and promote their apoptosis. Western blot and RT-PCR results showed that si-Notum can inhibit the Hedgehog signaling pathway. In addition, Notum human recombinant protein can increase the phosphorylation level of GSK3β and promote the expression of β-catenin, thereby further regulating the biological behavior of OSCC.Conclusions: Notum regulates the proliferation and migration of OSCC through Shh/p-GSK3β/β-catenin signaling pathway. Notum maybe an effective targets for the treatment of OSCC.

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Expression of Ki-67 and Βeta-Catenin in Pseudoepitheliomatous Hyperplasia and Squamous Cell Carcinoma in Oral Mucosal Biopsies : An Immunohistochemical Study

Cited by 9 publications

References 16 publications

An immunohistochemical study showing Ki-67 as an analytical marker in oral malignant and premalignant lesions

An immunohistochemical study showing Ki-67 as an analytical marker in oral malignant and premalignant lesions

Involvement of RUVBL1 in WNT/β-Catenin Signaling in Oral Squamous Cell Carcinoma

Notum Promotes Proliferation and Migration of Oral Squamous Cell Carcinoma Via Shh/p-GSK3β/β-Catenin Pathway

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