共查询到20条相似文献，搜索用时 15 毫秒
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Relapse cases of cancers are more vigorous and difficult to control due to the preponderance of cancer stem cells (CSCs). Such CSCs that had been otherwise dormant during the first incidence of cancer gradually appear as radiochemoresistant cancer cells. Hence, cancer therapeutics aimed at CSCs would be an effective strategy for mitigating the cancers during relapse. Alternatively, CSC therapy can also be proposed as an adjuvant therapy, along‐with the conventional therapies. As regenerative stem cells (RSCs) are known for their trophic effects, anti‐tumorogenicity, and better migration toward an injury site, this review aims to address the use of adult stem cells such as dental pulp derived; cord blood derived pure populations of regenerative stem cells for targeting CSCs. Indeed, pro‐tumorogenicity of RSCs is of concern and hence has also been dealt with in relation to breast CSC therapeutics. Furthermore, as notch signaling pathways are upregulated in breast cancers, and anti‐notch antibody based and sh‐RNA based therapies are already in the market, this review focuses the possibilities of engineering RSCs to express notch inhibitory proteins for breast CSC therapeutics. Also, we have drawn a comparison among various possibilities of breast CSC therapeutics, about, notch1 inhibition. J. Cell. Biochem. 119: 141–149, 2018. © 2017 Wiley Periodicals, Inc. 相似文献
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Payal Agarwal Maninder Sandey Patricia DeInnocentes R. Curtis Bird 《Journal of cellular biochemistry》2013,114(6):1355-1363
p16/INK4A/CDKN2A is an important tumor suppressor gene that arrests cell cycle in G1 phase inhibiting binding of CDK4/6 with cyclin D1, leaving the Rb tumor suppressor protein unphosphorylated and E2F bound and inactive. We hypothesized that p16 has a role in exit from cell cycle that becomes defective in cancer cells. Well characterized p16‐defective canine mammary cancer cell lines (CMT28, CMT27, and CMT12), derived stably p16‐transfected CMT cell clones (CMT27A, CMT27H, CMT28A, and CMT28F), and normal canine fibroblasts (NCF), were used to investigate expression of p16 after serum starvation into quiescence followed by re‐feeding to induce cell cycle re‐entry. The parental CMT cell lines used lack p16 expression either at the mRNA or protein expression levels, while p27 and other p16‐associated proteins, including CDK4, CDK6, cyclin D1, and Rb, were expressed. We have successfully demonstrated cell cycle arrest and relatively synchronous cell cycle re‐entry in parental CMT12, CMT28 and NCF cells as well as p16 transfected CMT27A, CMT27H, CMT28A, and CMT28F cells and confirmed this by 3H‐thymidine incorporation and flow cytometric analysis of cell cycle phase distribution. p16‐transfected CMT27A and CMT27H cells exited cell cycle post‐serum‐starvation in contrast to parental CMT27 cells. NCF, CMT27A, and CMT28F cells expressed upregulated levels of p27 and p16 mRNA, post‐serum starvation, as cells exited cell cycle and entered quiescence. Because quiescence and differentiation are associated with increased levels of p27, our data demonstrating that p16 was upregulated along with p27 during quiescence, suggests a potential role for p16 in maintaining these non‐proliferative states. J. Cell. Biochem. 114: 1355–1363, 2013. © 2012 Wiley Periodicals, Inc. 相似文献
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Cornelia Johanna Franziska Scheitz Tudorita Tumbar 《Journal of cellular biochemistry》2013,114(5):985-993
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Caiyu Lin Li Wang Hong Wang Liuqi Yang Huijie Guo Xiujie Wang 《Journal of cellular biochemistry》2013,114(9):2061-2070
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Shambhavi Naik Marion MacFarlane Apurva Sarin 《Journal of cellular biochemistry》2015,116(7):1371-1380
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Feng Wang Frank Stappenbeck William Matsui Farhad Parhami 《Journal of cellular biochemistry》2017,118(3):499-509
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Andrew Fritz Seema Sinha Narasimharao Marella Ronald Berezney 《Journal of cellular biochemistry》2013,114(5):1074-1083
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Adam Albitar Bahar Rohani Brett Will Annie Yan G. Ian Gallicano 《Journal of cellular biochemistry》2018,119(1):134-140
CRISPR/Cas gene editing technologies have emerged as powerful tools in the study of oncogenic transformation. The system's specificity, versatility, and ease of implementation allow researchers to identify important molecular markers and pathways which grant cancers stem cell like properties. This technology has already been applied to researching specific cancers, but has seen restricted therapeutic applications due to inherent ethical and technical limitations. Active development and adaptation of the CRISPR/Cas system has produced new methods to take advantage of both non‐homologous end joining and homologous recombination repair mechanisms in attempts to remedy these limitations and improve the versatility of gene edits that can be created. Nonetheless, until issues with specificity and in vivo efficiency are resolved, utilization of CRISPR/Cas systems would be best employed in the modeling and study of various cancer genes. While it may have potential therapeutic applications to targeted cancer therapies in the future, presently CRISPR/Cas is a remarkable technique that can be utilized for easy and efficient gene editing when it comes to cancer research. J. Cell. Biochem. 119: 134–140, 2018. © 2017 Wiley Periodicals, Inc. 相似文献
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Wang S Li W Liu N Zhang F Liu H Liu F Liu J Zhang T Niu Y 《Journal of cellular biochemistry》2012,113(6):1904-1914
Nek2A (NIMA-related kinases 2A) has been known as an important centrosome regulatory factor. The aim of this study was to investigate the expression of Nek2A and the role it played in different stages of breast cancer. We detected the expression of Nek2A in both mRNA and protein levels in MCF10 cell lines including MCF-10A, MCF-10DCIS.com, MCF-10CA1a and in human breast samples which contained normal breast tissue (NBT), breast ductal carcinoma in situ (DCIS), and invasive ductal carcinoma (IDC). Our study revealed that the mRNA and protein expression of Nek2A were significantly up-regulated in MCF-10DCIS.com and MCF-10CA1a cell lines as well as in human primary breast cancer tissue (DCIS and IDC). Our study also presented a correlation between Nek2A mRNA expression and some clinic pathological factors. We found that Nek2A mRNA expression was associated with molecular subtypes, ER, PR and Ki-67 immunoreactivity (P<0.05) in DCIS and associated with histological grade, lymph node metastasis, molecular subtypes, c-erbB-2, and Ki-67 expression (P<0.05) in IDC. In addition, we observed that ectopic expression of Nek2A in \"normal\" immortalized MCF-10A breast epithelial cell resulted in increased Nek2A which lead to abnormal centrosomes. Furthermore, knockdown of Nek2A in MCF-10DCIS.com could remarkably inhibit cell proliferation and induce cell cycle arrest in MCF-10DCIS.com cell line. These data suggested that Nek2A might bear a close relationship with development and progression of breast carcinoma, and highlighted its role as a novel potential biomarker for diagnosis and a possible therapeutic target for human breast cancer especially for DCIS. 相似文献
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Tae‐Ho Kang Ji‐Hye Seo Hana Oh Goo Yoon Jung‐Il Chae Jung‐Hyun Shim 《Journal of cellular biochemistry》2017,118(12):4652-4663
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Hao Daniel Lin Chui‐Yee Fong Arijit Biswas Mahesh Choolani Ariff Bongso 《Journal of cellular biochemistry》2016,117(9):2045-2055
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De Luca A Lamura L Gallo M Maffia V Normanno N 《Journal of cellular biochemistry》2012,113(11):3363-3370
Several different cytokines and growth factors secreted by mesenchymal stem cells (MSCs) have been hypothesized to play a role in breast cancer progression. By using a small panel of breast cancer cell lines (MCF‐7, T47D, and SK‐Br‐3 cells), we analyzed the role of interleukin‐6 (IL‐6) and vascular endothelial growth factor A (VEGF) in the cross‐talk between MSCs and breast cancer cells. We performed migration assays in which breast cancer cells were allowed to migrate in response to conditioned medium from MSCs (MSCs‐CM), in absence or in presence of the anti‐VEGF antibody bevacizumab or an anti‐IL‐6 antibody, alone or in combination. We found that anti‐VEGF and anti‐IL‐6 antibodies inhibited the migration of breast cancer cells and that the combination had an higher inhibitory effect. We next evaluated the effects of recombinant VEGF and IL‐6 proteins on breast cancer cell growth and migration. IL‐6 and VEGF had not significant effects on the proliferation of breast carcinoma cells. In contrast, both VEGF and IL‐6 significantly increased the ability to migrate of MCF‐7, T47D and SK‐Br‐3 cells, with the combination showing a greater effect as compared with treatment with a single protein. The combination of VEGF and IL‐6 produced in breast cancer cells a more significant and more persistent activation of MAPK, AKT, and p38MAPK intracellular signaling pathways. These results suggest that MSC‐secreted IL‐6 and VEGF may act as paracrine factors to sustain breast cancer cell migration. J. Cell. Biochem. 113: 3363–3370, 2012. © 2012 Wiley Periodicals, Inc. 相似文献