Effect of thalidomide in combination with gemcitabine on human pancreatic carcinoma SW-1990 cell lines in vitro and in vivo

Qiao, Zhenguo; Yuan, Jigang; Shen, Jiaqing; Wang, Chao; He, Zhilong; Hu, Yijia; Zhang, Muxing; Xu, Chunfang

doi:10.3892/ol.2015.3064

Cited by 8 publications

(6 citation statements)

References 32 publications

(29 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, there are little or no effective benefits obtained from mono-therapies with thalidomide or its analogs in the treatment of solid tumors. Recently, thalidomide combined with typical chemotherapeutic drugs or immunomodulatory drugs showed curative effects in pre-clinical studies of tumor and leukemia [ 30 , 31 ]. Our presented study developed a combination of thalidomide with icotinib which showed distinctly synergic cytostatic and pro-apoptotic effects in lung cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Synergistic Inhibition of Thalidomide and Icotinib on Human Non-Small Cell Lung Carcinomas Through ERK and AKT Signaling

et al. 2018

View full text Add to dashboard Cite

BackgroundEpidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) have been widely used in the treatment of non-small cell lung cancer (NSCLC) patients with sensitive EGFR mutations. However, the survival of patients with EGFR-TKI administration is limited by the inevitable development of acquired drug resistance. Recently, multi-targeted drugs combination has been shown to be a promising strategy to improve the efficacy of EGFR-TKI treatment and enable the reduction of drug resistance in NSCLC.Material/MethodsHumanized NSCLC cell lines PC9 and A549 were co-cultured with thalidomide and/or icotinib to test for anti-tumor efficiency. Cell proliferation was measured by MTT assay, cell apoptosis by flow cytometry and cell migration by wound healing assay. Western blot was performed to determine the expression of caspase-3, -8, -9, Bax, EGFR, VEGF-R, AKT, ERK, MMP2, MMP9, and NF-κB. The xenograft mouse model was used to explore the effects of thalidomide and icotinib in vivo. Immunohistochemical testing was used to determine the expression of Ki-67 and TUNEL staining in tumor tissues.ResultsTreatments of thalidomide and/or icotinib reduced cell viability, induced apoptosis, and suppressed migration. Attenuation of pEGFR and pVEGF-R resulted in deactivation of ERK and AKT pathways, which eventually increased the anti-proliferative response. In PC9 xenograft model, combined administration of thalidomide and icotinib restrained tumor growth with remarkable reduced Ki-67 index and increased TUNEL positive cells.ConclusionsThalidomide sensitizes icotinib to increase apoptosis and prevent migration, and it may be a potentially promising anti-tumor drug in lung cancer multi-modality therapy.

show abstract

Section: Discussionmentioning

confidence: 99%

Synergistic Inhibition of Thalidomide and Icotinib on Human Non-Small Cell Lung Carcinomas Through ERK and AKT Signaling

et al. 2018

View full text Add to dashboard Cite

show abstract

“…2B ). BCL-2 is an anti-apoptotic protein, whereas BAX promotes apoptosis ( 37 ). In the present study, the protein expression levels of anti-apoptotic protein BCL-2 were downregulated with increased THD concentration, whereas the protein expression levels of pro-apoptotic protein BAX and cleaved-caspase-3 were upregulated compared with the control group ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Vascular endothelial growth receptor 1 acts as a stress‑associated protein in the therapeutic response to thalidomide

et al. 2017

View full text Add to dashboard Cite

Thalidomide (THD) exhibits antitumor effects in several types of cancer. However, the failure of THD to inhibit tumor growth has also been observed in a number of murine models in vivo. The mechanism involved in the therapeutic failure of THD remains unclear. The present study demonstrated that, accompanied by growth-arresting and apoptosis-inducing effects (P<0.05), THD upregulated vascular endothelial growth factor receptor 1 (VEGFR1) expression levels in CT26 murine colorectal carcinoma cell lines. This in vitro phenomenon was also observed in various other cell lines, including human umbilical vein endothelial cells, SW480, SW620 and HCT116. Reactive oxygen species (ROS) levels were increased compared with those in the untreated control when cells were exposed to THD (P<0.05). Furthermore, results suggested that ROS suppression may have provoked the induction of VEGFR1 expression to some extent. In addition, the results revealed that THD failed to inhibit CT26 tumor growth in vivo and the expression of VEGFR1 protein was elevated by THD treatment compared with the control group in the murine colorectal tumor model (P<0.05). The results of further experiments suggested that VEGFR1 was elevated in response to various stress-associated situations, including chemotherapy, radiotherapy and thermotherapy, which indicate that it may act as a stress-associated protein. The present findings provide a foundation for the future study of VEGFR1-targeted therapy to enhance the efficacy of current therapies.

show abstract

“…Qiao et al (40) demonstrated that the expression of Bax mRNA was upregulated, the expression of Bcl-2 gene was downregulated following the treatment of SW1990 pancreatic cancer cells with THD.…”

Section: Discussionmentioning

confidence: 99%

Effects of thalidomide on growth and VEGF-A expression in SW480 colon cancer cells

Zhang

Luo

2017

Oncol Lett

View full text Add to dashboard Cite

Abstract. Lymphatic and hematogenous spread are the most common ways for tumors to metastasize. Angiogenesis is essential for tumor growth and metastasis. Vascular endothelial growth factor (VEGF) particularly VEGF-A is important in the process of angiogenesis. The current research has indicated that thalidomide (THD) may be able to inhibit angiogenesis, stimulate the activity of the immune system and inhibit the adherence of cancer cells to stromal cells. These changes may lead to suppression of tumor occurrence and development. To date, to the best of our knowledge, the effects of THD on colon cancer SW480 cells have not been reported. In the present study, the effects of THD and a combination of THD and oxaliplatin (L-OHP) on the proliferation of SW480 cells have been investigated. Furthermore, the expression of VEGF-A and hypoxia-inducible factor 1 (HIF-1) was analyzed using MTT assay, quantitative polymerase chain reaction and western blot analysis. The results indicated that THD was able to inhibit SW480 cells in dose-and-time dependent manner and inhibit the expression of VEGF-A and HIF-1α. Furthermore, treatment with THD and L-OHP had synergistic inhibitory effect, which may provide a novel treatment strategy for advanced colorectal cancer.

show abstract

Effect of thalidomide in combination with gemcitabine on human pancreatic carcinoma SW-1990 cell lines in vitro and in vivo

Cited by 8 publications

References 32 publications

Synergistic Inhibition of Thalidomide and Icotinib on Human Non-Small Cell Lung Carcinomas Through ERK and AKT Signaling

Synergistic Inhibition of Thalidomide and Icotinib on Human Non-Small Cell Lung Carcinomas Through ERK and AKT Signaling

Vascular endothelial growth receptor 1 acts as a stress‑associated protein in the therapeutic response to thalidomide

Effects of thalidomide on growth and VEGF-A expression in SW480 colon cancer cells

Contact Info

Product

Resources

About