Silencing of mutant p53 by siRNA induces cell cycle arrest and apoptosis in human bladder cancer cells

Zhu, Hai‐Bin; Yang, Kai; Xie, Yanqi; Lin, Yiwei; Mao, Qinan; Xie, Liping

doi:10.1186/1477-7819-11-22

Cited by 53 publications

(36 citation statements)

References 46 publications

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“…Recently, RNA interference has been extensively used to target genes implicated with proliferation, apoptosis, cell cycle regulation, invasion, and metastasis in bladder cancer, [21][22][23][24][25][26][27] which provides promising therapeutic strategies for the treatment of bladder cancer. In the present study, the authors employed lentivirus-mediated RNAi to suppress SKA1 expression in BT5637 and T-24 bladder cancer cell lines.…”

Section: Discussionmentioning

confidence: 99%

Downregulation ofSKA1Gene Expression Inhibits Cell Growth in Human Bladder Cancer

Tian

Xing

et al. 2015

Cancer Biotherapy and Radiopharmaceuticals

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Spindle and kinetochore-associated protein 1 (SKA1), a component of microtubule-binding complex of kinetochore, is essential for proper chromosome segregation. Recently, SKA1 has been shown to be involved in malignant progression of several human cancers. However, its role in bladder cancer is still unknown. To evaluate the function of SKA1 in bladder cancer cells, the authors employed an RNA interference lentivirus system to deplete its expression in both BT5637 and T-24 bladder cancer cells. The cell proliferation was significantly decreased in both cell lines after SKA1 knockdown. Moreover, the colony formation capacity was impaired by SKA1 silencing. Flow cytometry analysis showed that depletion of SKA1 led to cell cycle arrest at S phase. Furthermore, knockdown of SKA1 in T-24 cells obviously downregulated the expressions of CDK4 and Cyclin D1, and alleviated the activations of ERK2 and AKT, conducive to cell growth inhibition. These findings suggested that knockdown of SKA1 could potently suppress bladder cancer cell proliferation in vitro and lentivirus-mediated silencing of SKA1 might serve as a novel strategy for gene therapy of bladder cancer.

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Section: Discussionmentioning

confidence: 99%

Downregulation ofSKA1Gene Expression Inhibits Cell Growth in Human Bladder Cancer

Tian

Xing

et al. 2015

Cancer Biotherapy and Radiopharmaceuticals

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“…Studies have indicated that knockdown of mutant p53 by siRNA was able to induce G2-phase cell cycle arrest and apoptosis in human bladder cancer cells. Moreover, this strategy cooperated with cisplatin in the inhibition of cancer cells37.…”

Section: Discussionmentioning

confidence: 99%

The impact of p53 in predicting clinical outcome of breast cancer patients with visceral metastasis

Yang

Kwan

et al. 2013

Sci Rep

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In the study, we analyzed role of p53 in predicting outcome in visceral metastasis breast cancer (VMBC) patients. 97 consecutive VMBC patients were studied. P53 positivity rate was 29.9%. In the p53-negative group, median disease free survival (DFS), and time from primary breast cancer diagnosis to death (OS1), time from metastases to death (OS2) were 25, 42.5, and 13.5 months, respectively. In the p53-positive group, they were 10, 22, and 8 months, respectively. Statistically significant differences in DFS and OS1 were detected between the p53-negative and p53-positive subtypes. However, p53 appears to have no influence on OS2. In Cox regression analysis, p53 expression and TNM stage were predictive factors of DFS. In the multivariate analysis, p53 expression and the duration of DFS correlated with OS1, but not for OS2. Taken together, our data indicate p53 showing predicting role in OS1 for VMBC, but not for OS2.

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“…Given that stabilization of mutant p53 is required for its GOF activities [11,58,64,65,66,67], our study reveals a novel mechanism by which the mevalonate pathway contributes to cancer progression. Thus, the mevalonate pathway promotes tumorigenesis by two mechanisms: (1) by enhancing protein prenylation, which is required for the activation of proteins involved in proliferation and migration, such as Ras and Rho; and (2) by stabilizing conformational mutant p53.…”

Section: Summary and Future Perspectivesmentioning

confidence: 98%

p53 as a Regulator of Lipid Metabolism in Cancer

Parrales

Iwakuma

2016

IJMS

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Enhanced proliferation and survival are common features of cancer cells. Cancer cells are metabolically reprogrammed which aids in their survival in nutrient-poor environments. Indeed, changes in metabolism of glucose and glutamine are essential for tumor progression. Thus, metabolic reprogramming is now well accepted as a hallmark of cancer. Recent findings suggest that reprogramming of lipid metabolism also occurs in cancer cells, since lipids are used for biosynthesis of membranes, post-translational modifications, second messengers for signal transduction, and as a source of energy during nutrient deprivation. The tumor suppressor p53 is a transcription factor that controls the expression of proteins involved in cell cycle arrest, DNA repair, apoptosis, and senescence. p53 also regulates cellular metabolism, which appears to play a key role in its tumor suppressive activities. In this review article, we summarize non-canonical functions of wild-type and mutant p53 on lipid metabolism and discuss their association with cancer progression.

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Silencing of mutant p53 by siRNA induces cell cycle arrest and apoptosis in human bladder cancer cells

Cited by 53 publications

References 46 publications

Downregulation ofSKA1Gene Expression Inhibits Cell Growth in Human Bladder Cancer

Downregulation ofSKA1Gene Expression Inhibits Cell Growth in Human Bladder Cancer

The impact of p53 in predicting clinical outcome of breast cancer patients with visceral metastasis

p53 as a Regulator of Lipid Metabolism in Cancer

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