Knockdown of Ki-67 by small interfering RNA leads to inhibition of proliferation and induction of apoptosis in human renal carcinoma cells

Zheng, Junnian; Ma, Tianzhou; Cao, Jingyi; Sun, Xiaofang; Chen, Jiacun; Li, Wang; Wen, Rumin; Sun, Yeqing; Pei, Dong‐Sheng

doi:10.1016/j.lfs.2005.05.064

Cited by 45 publications

(42 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…14,15 We wish to improve these results by using shRNA delivered by the adenoviral vector for a more effective, stable and long-term RNAi. Indeed, it has been proven that non-replicating adenoviral vectors expressing shRNAs could induce silencing of target genes in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of renal cancer cell growth in vitro and in vivo with oncolytic adenovirus armed short hairpin RNA targeting Ki-67 encoding mRNA

Zheng

Park

et al. 2008

Cancer Gene Ther

View full text Add to dashboard Cite

RNA interference (RNAi) has been proved to be a powerful tool for gene knockdown purpose and holds great promise for the treatment of cancer. Our previous study demonstrated that the reduction of Ki-67 expression by means of chemically synthesized siRNAs and shRNAs expressed from plasmid resulted in proliferation inhibition in human renal carcinoma cells. In this study, we constructed a novel oncolytic adenovirus-based shRNA expression system, ZD55-Ki67, and explored ZD55-Ki67-mediated RNAi for Ki-67 gene silencing. Our results showed that ZD55-Ki67 could induce silencing of the Ki-67 gene effectively, allow for efficient tumor-specific viral replication and induce the apoptosis of tumor cells effectively in vitro and in nude mice. We conclude that combining shRNA gene therapy and oncolytic virotherapy can enhance antitumor efficacy as a result of synergism between CRAd oncolysis and shRNA antitumor responses.

show abstract

Section: Discussionmentioning

confidence: 99%

Inhibition of renal cancer cell growth in vitro and in vivo with oncolytic adenovirus armed short hairpin RNA targeting Ki-67 encoding mRNA

Zheng

Park

et al. 2008

Cancer Gene Ther

View full text Add to dashboard Cite

show abstract

“…Yoa et al, [16] reported that among many of the cancer-related genes tested, that of Ki-67 expression was one of the highest in rat bladder tumors, reaching nearly 20-fold higher levels compared to normal tissue. Thus, Ki-67 has been one of the genes of interest to target, using AsODNs [17], [18] or siRNAs [19], [20]. In more recent report, AsODN against Ki-67 was used in Phase-I clinical trials for the treatment of human bladder cancer [21].…”

Section: Introductionmentioning

confidence: 99%

Knockdown of Ki-67 by Dicer-Substrate Small Interfering RNA Sensitizes Bladder Cancer Cells to Curcumin-Induced Tumor Inhibition

et al. 2012

View full text Add to dashboard Cite

Transitional cell carcinoma (TCC) of the urinary bladder is the most common cancer of the urinary tract. Most of the TCC cases are of the superficial type and are treated with transurethral resection (TUR). However, the recurrence rate is high and the current treatments have the drawback of inducing strong systemic toxicity or cause painful cystitis. Therefore, it would be of therapeutic value to develop novel concepts and identify novel drugs for the treatment of bladder cancer. Ki-67 is a large nucleolar phosphoprotein whose expression is tightly linked to cell proliferation, and curcumin, a phytochemical derived from the rhizome Curcuma longa, has been shown to possess powerful anticancer properties. In this study, we evaluated the combined efficacy of curcumin and a siRNA against Ki-67 mRNA (Ki-67-7) in rat (AY-27) and human (T-24) bladder cancer cells. The anticancer effects were assessed by the determination of cell viability, apoptosis and cell cycle analysis. Ki-67-7 (10 nM) and curcumin (10 µM), when treated independently, were moderately effective. However, in their combined presence, proliferation of bladder cancer cells was profoundly (>85%) inhibited; the rate of apoptosis in the combined presence of curcumin and Ki-67-7 (36%) was greater than that due to Ki-67-7 (14%) or curcumin (13%) alone. A similar synergy between curcumin and Ki-67-7 in inducing cell cycle arrest was also observed. Western blot analysis suggested that pretreatment with Ki-67-7 sensitized bladder cancer cells to curcumin-mediated apoptosis and cell cycle arrest by p53- and p21-independent mechanisms. These data suggest that a combination of anti-Ki-67 siRNA and curcumin could be a viable treatment against the proliferation of bladder cancer cells.

show abstract

“…The Ki-67 protein has been shown to be necessary for cell proliferation, as well as ribosomal RNA transcription [36]. Studies have shown that inhibition of Ki-67 leads to both a decrease in ribosomal RNA transcription and an increase in apoptosis [37,38]. Since the rats from the MTrxMI group showed significantly better outcomes across all parameters compared to the MLZMI group, it is clear that the MSCs preconditioned with Ad.Trx1 provided enhanced cardioprotection.…”

Section: Discussionmentioning

confidence: 99%

Thioredoxin-1 (Trx1) engineered mesenchymal stem cell therapy increased pro-angiogenic factors, reduced fibrosis and improved heart function in the infarcted rat myocardium

Suresh

Selvaraju

Thirunavukkarasu

et al. 2015

International Journal of Cardiology

View full text Add to dashboard Cite

Knockdown of Ki-67 by small interfering RNA leads to inhibition of proliferation and induction of apoptosis in human renal carcinoma cells

Cited by 45 publications

References 28 publications

Inhibition of renal cancer cell growth in vitro and in vivo with oncolytic adenovirus armed short hairpin RNA targeting Ki-67 encoding mRNA

Inhibition of renal cancer cell growth in vitro and in vivo with oncolytic adenovirus armed short hairpin RNA targeting Ki-67 encoding mRNA

Knockdown of Ki-67 by Dicer-Substrate Small Interfering RNA Sensitizes Bladder Cancer Cells to Curcumin-Induced Tumor Inhibition

Thioredoxin-1 (Trx1) engineered mesenchymal stem cell therapy increased pro-angiogenic factors, reduced fibrosis and improved heart function in the infarcted rat myocardium

Contact Info

Product

Resources

About