Angiogenesis during tumor progression in the oral cavity is related to reduced apoptosis and high tumor cell proliferation

Ravi, Devendra Kumar; Ramadas, K; Mathew, Babu; Nalinakumari, K.R.; Nair, Muralidharan; Pillai, M. Radhakrishna

doi:10.1016/s1368-8375(98)00054-2

Cited by 42 publications

(35 citation statements)

References 25 publications

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“…The proliferation rate and growth patterns of tumors have significant impacts on disease development and prognosis of the patients; indeed, the proliferation rate of tumor cells can indirectly reflect the tumor malignancy (Ravi et al, 1998). Proliferation of malignant cells can be affected by changes in many different proteins, but evidence indicates that the CXCL12-CXCR4 biological axis is important to this process (Chen et al, 2006;Li et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

CXCL12-CXCR4 Promotes Proliferation and Invasion of Pancreatic Cancer Cells

Shen

Zheng²,

Lu³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Objective: CXCL12 exerts a wide variety of chemotactic effects on cells. Evidence indicates that CXCL12, in conjunction with its receptor, CXCR4, promotes invasion and metastasis of tumor cells. Our objective was to explore whether the CXCL12-CXCR4 biological axis might influence biological behavior of pancreatic cancer cells. Methods: Miapaca-2 human pancreatic cancer cells were cultured under three different conditions: normal medium (control), medium + recombinant CXCL12 (CXCL12 group), or medium + CXCR4-inhibitor AMD3100 (AMD3100 group). RT-PCR was applied to detect mRNA expression levels of CXCL12, CXCR4, matrix metalloproteinase 2 (MMP-2), MMP-9, and human urokinase plasminogen activator (uPA). Additionally, cell proliferation and invasion were performed using CCK-8 colorimetry and transwell invasion assays, respectively. Results: CXCL12 was not expressed in Miapaca-2 cells, but CXCR4 was detected, indicating that these cells are capable of receiving signals from CXCL12. Expression of extracellular matrix-degrading enzymes MMP-2, MMP-9, and uPA was upregulated in cells exposed to exogenous CXCL12 (P<0.05). Additionally, both proliferation and invasion of pancreatic cancer cells were enhanced in the presence of exogenous CXCL12, but AMD3100 intervention effectively inhibited these processes (P<0.05). Conclusions: The CXCL12-CXCR4 biological axis plays an important role in promoting proliferation and invasion of pancreatic cancer cells.

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Section: Discussionmentioning

confidence: 99%

CXCL12-CXCR4 Promotes Proliferation and Invasion of Pancreatic Cancer Cells

Shen

Zheng²,

Lu³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…This fact can indicate a deregulation of the apoptosis mechanisms in oral lichen planus, preventing the death of genetically damaged cells and consequently, increasing the malignant transformation risk (27). Some studies suggested that decrease in the expression of bax is essential for the development and progression of oral cancer (14,17,19,28). Although bax and bcl-2 are strongly associated in apoptosis, no correlation between these proteins was observed in this study, which can be explained by the existence of different mechanisms of apoptosis regulation.…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical expression of PCNA, p53, bax and bcl-2 in oral lichen planus and epithelial dysplasia

et al. 2009

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A b s t r a c t : T h e p o t e n t i a l fo r m a l i g n a n t transformation of oral lichen planus is still controversial.The expression of proteins related to cell proliferation and apoptosis in oral lichen planus and epithelial dysplasia was analyzed to evaluate the true potential for malignant transformation of this disease. Twentyfour cases of each lesion were subjected to the streptoavidin-biotin technique for identifying the immunohistochemical expression of PCNA, p53, bax, and bcl-2 proteins. Of the 24 cases of oral lichen planus, 14 (58.33%) were positive for PCNA, 10 (41.67%) for p53, 4 (16.67%) for bcl-2 and 12 (50%) for bax, whereas of the 24 cases of epithelial dysplasia, 20 (83.33%) were positive for PCNA, 10 (41.67%) for p53, 6 (25%) for bcl-2, and 20 (83.33%) for bax. Chi-squared test showed no statistically significant differences between the expression of p53 and bcl-2 in oral lichen planus and epithelial dysplasia, regardless of the grade (P > 0.05). However, the expression of PCNA and bax was significantly increased in epithelial dysplasia (P < 0.05). The results of this study showed that alterations in expression of these proteins are observed in oral lichen planus and epithelial dysplasia, suggesting the potential for malignant transformation in both lesions. IntroductionOral lichen planus is a chronic inflammatory disease of unknown cause, and its potential for malignant transformation is a subject of much controversy (1). Since the first case was reported in 1910, several studies have suggested that patients with oral lichen planus are at an increased risk of developing cancer (1-7).However, many authors believe that there is insufficient data to prove an association between oral lichen planus and cancer. For these authors, most cases of malignant transformation are the result of errors in the initial diagnosis of the disease (1,8-13).The true potential for malignant transformation of oral lichen planus can be evaluated by analyzing the expression of proteins related to cell proliferation and apoptosis, as alterations in the expression of these proteins are essential for carcinogenesis (14)(15)(16)(17)(18)(19).Therefore, the aim of this study was to evaluate the immunohistochemical expression of PCNA, p53, bax and bcl-2 proteins in oral lichen planus and epithelial dysplasia in order to explain the controversy regarding the potential for malignant transformation of oral lichen planus and emphasize the importance of long-term follow-up of patients with this disease. Materials and MethodsThe samples used in this study consisted of 24 cases of oral lichen planus and 24 cases of epithelial dysplasia (4 mild, 12 moderate, 8 severe) obtained from the records of

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“…Immunocytochemistry was carried out as described by us earlier (9,10). All sections were processed for antigen retrieval using Target Unmasking Fluid (TUF, Kreatech, Amsterdam, The Netherlands).…”

Section: Immunocytochemistry For P53 Ki 67 and E6 Expressionmentioning

confidence: 99%

“…Expression of p53, cyclin D1 and Ki 67 was considered significant when characteristic nuclear immunoreactivity was seen in at least 10% of the tumor cells. In addition to this, an expression index was also created as described by us earlier (9,10). This was done by classifying the protein expression into four categories.…”

Section: Immunocytochemistry For P53 Ki 67 and E6 Expressionmentioning

confidence: 99%