Companied P16 genetic and protein status together providing useful information on the clinical outcome of urinary bladder cancer

Pu, Xiaohong; Zhu, Liya; Fu, Yao; Fan, Zhiwen; Zheng, Jinyu; Zhang, Biao; Yang, Jun; Guan, Wenyan; Wu, Hongyan; Ye, Qing; Qing, Huang

doi:10.1097/md.0000000000010353

Cited by 7 publications

(4 citation statements)

References 41 publications

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“…In addition, p16 is a cyclin dependent inhibitor (CDI), which can negatively regulate the cell cycle by inhibiting CDK (50,52,53). The inactivation of the p16 gene will lead to excessive cell proliferation (54). Thus, we hypothesized that p16 may affect cell proliferation in OS.…”

Section: Discussionmentioning

confidence: 99%

miR‑9 depletion suppresses the proliferation of osteosarcoma cells by targeting p16

et al. 2019

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Osteosarcoma (OS) is a common primary malignancy in adolescents and children. MicroRNAs (miRNAs or miRs) can regulate the progression of OS. Herein, we explored the target genes and effects of miR-9 in OS. Cell growth, colony formation and cell cycle were respectively examined using a cell counting kit-8 (CCK-8), crystal violet staining and flow cytometry. The target gene of miR-9 was predicted according to the MicroRNA.org website. Luciferase activity was examined using a dual luciferase reporter gene assay kit. The corresponding factors levels were analyzed by carrying out reverse transcription-quantitative PCR (RT-qPCR) and western blot analysis. A mouse model of OS was also established and the volume and weight of the tumors of the mice with OS were measured. The levels of p16 in the mice with OS were detected by immunohistochemistry (IHC). The data revealed a high expression of miR-9 and a low expression of p16 in the OS tissue. p16 was found to be the target gene for miR-9 in OS. miR-9 depletion decreased the proliferation and colony formation of Saos-2 cells by arresting the cells at the G1 phase, accompanied by the downregulation of cyclin A, cyclin D1 and c-Myc expression levels. Moreover, miR-9 depletion inhibited the phosphorylation of p38, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK). In vivo , miR-9 depletion decreased the tumor volume and weight and increased p16 expression in the mouse tumor tissues. Nevertheless, p16 silencing reversed the suppressive effects of miR-9 inhibitors on OS cells. On the whole, the findings of this study substantiate that miR-9 depletion suppresses cell proliferation by targeting p16 in OS and by mediating the activation of the ERK/p38/JNK pathway.

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Section: Discussionmentioning

confidence: 99%

miR‑9 depletion suppresses the proliferation of osteosarcoma cells by targeting p16

et al. 2019

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“…Feng et al (9) found that when the expression level of p16 is blocked, it leads to dominant binding between cyclin D1 and CDK4 and continuous cell proliferation, thus resulting in tumors. According to the study of Pu et al (10), p16 is a predisposing gene of cardiac carcinoma, and it has been shown in several animal models that the p16 expression level in cardiac carcinoma tissues is significantly reduced. However, the correlation of p16 and cyclin D1 with incidence and prognosis of cardiac carcinoma remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Correlation of p16 and cyclin D1 expression with the incidence and prognosis of cardiac carcinoma

Wang

Wang²,

Zhao

2019

Oncol Lett

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Correlation of p16 and cyclin D1 expression with the incidence and prognosis of cardiac carcinoma was investigated. Thirty-six patients with cardiac carcinoma treated in The Second Affiliated Hospital of Zhengzhou University were selected. After the radical operation of cardiac carcinoma, carcinoma tissues were taken, and the corresponding para-carcinoma tissues were used as controls. p16 and cyclin D1 messenger ribonucleic acid (mRNA) and protein expression in cardiac carcinoma tissues and para-carcinoma tissues were detected via quantitative polymerase chain reaction (qPCR) and western blot analysis. The survival time and pathological conditions of patients with cardiac carcinoma were recorded in detail, and correlation of p16 and cyclin D1 with incidence and prognosis of cardiac carcinoma was studied. In cardiac carcinoma tissues, the p16 mRNA and protein expression levels were significantly lower than those in para-carcinoma tissues (P<0.01), but the cyclin D1 mRNA and protein expression levels were significantly higher than those in para-carcinoma tissues (P<0.01). The expression of p16 and cyclin D1 protein had correlation with the tumor size, lymph node metastasis and tumor-node-metastasis stage of cardiac carcinoma (P<0.01). There was a negative correlation between expression of p16 and cyclin D1 in cardiac carcinoma (P<0.01). According to Kaplan-Meier survival analysis, the survival rate of patients with high expression of p16 was obviously higher than that of patients with low expression of p16 (P<0.01), while the survival rate of patients with high expression of cyclin D1 was obviously lower than that of patients with low expression of cyclin D1 (P<0.01). Both p16 and cyclin D1 are closely related to the incidence and prognosis of cardiac carcinoma, which may become indexes for the incidence and prognosis of cardiac carcinoma.

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“…Hashmi et al concluded that high p16 expression was associated with higher grade and muscle invasion [ 58 ]. Some authors found that neither p16 gene status nor the p16 protein expression alone can be nominated as an independent predictor for urothelial carcinomas, but combining protein and gene status together provides useful information on such clinical outcomes of these patients [ 59 ]. We did not find a significant difference between MIBC and NIBC or between both grades except when differentiating between the papillary group and non-papillary, where the papillary lesions showed a significant difference between p16 expression in high grade compared to the low grade and in MIBC versus NMIBC which may raise the attention of histological pattern significance in conventional UCs.…”

Section: Discussionmentioning

confidence: 99%

Clinico-Pathological Features and Immunohistochemical Comparison of p16, p53, and Ki-67 Expression in Muscle-Invasive and Non-Muscle-Invasive Conventional Urothelial Bladder Carcinoma

Hasan,

Mohammed,

Basiony

et al. 2023

Clinics and Practice

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Introduction: The identification of bladder detrusor muscle invasion in urothelial cancer is essential for prognosis and management. We studied the clinical, histological, and immunohistochemical expression of p16, p53, and Ki-67 in urothelial detrusor muscle-invasive bladder cancer (MIBC) and urothelial non-detrusor muscle-invasive bladder cancer (NMIBC) in Egyptian patients. Methods: Sixty-two bladder urothelial cancer cases obtained through TURBT were included and divided into two groups: (MIBC, stage T2) and NMIBC (T1). Tissue blocks were recut and re-examined microscopically; then, the immunostaining of p16, p53, and Ki-67 was performed to compare both groups and evaluate the 13% cut-off for Ki-67, 20% for p53, and p16 intensity in various conditions aided by telepathology technology. Results and conclusion: Hematuria was the main clinical first presentation, with no significant difference between either group. The mean age was 61.6 years, with male predominance (52 males and 10 females). The absence of papillary histological pattern was associated with a higher stage, including detrusor muscle invasion (p = 0.000). The overall average percent of p53 immunostaining was 12.9%, revealing no significant difference between MIBC and NMIBC when a cut-off of 20% was implicated. The Ki-67 expression was correlated with higher grade and muscle invasion; however, no association was found with the other two markers’ expression. The negative immunostaining of p16 was associated with low grade and NMIBC in the case of the preservation of the papillary pattern. We recommend further studies on the cut-off of widely used markers and more immunohistochemical and genetic studies on the p16(INK4A), taking into consideration the histological pattern of conventional carcinomas.

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Companied P16 genetic and protein status together providing useful information on the clinical outcome of urinary bladder cancer

Cited by 7 publications

References 41 publications

miR‑9 depletion suppresses the proliferation of osteosarcoma cells by targeting p16

miR‑9 depletion suppresses the proliferation of osteosarcoma cells by targeting p16

Correlation of p16 and cyclin D1 expression with the incidence and prognosis of cardiac carcinoma

Clinico-Pathological Features and Immunohistochemical Comparison of p16, p53, and Ki-67 Expression in Muscle-Invasive and Non-Muscle-Invasive Conventional Urothelial Bladder Carcinoma

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