“…In addition, KLT pretreatment enhanced the upregulation of survivin expression caused by Taxol, and the “KLT+Taxol” group had the highest survivin expression. These results are consistent with those reported in other studies 27, 28 .Figure 4Western blotting results of cyclin B1, survivin, Cx43, caspase-3, PARP and caspase-8 in four colorectal cancer cell lines, HCT106, HCT116, LoVo, and CT26, which were treated with different combinations of drugs. β-Actin or GAPDH was used as a loading control.…”
Taxol, a first-line anti-tumour drug, has low effectiveness against colorectal cancer. Combination with other agents is an effective strategy to enhance Taxol cytotoxicity. Kanglaite injection is an extract from Coix lacryma-jobi seed and is usually combined with other agents to treat cancer. The aim of this study was to investigate the treatment effect of Taxol combined with Kanglaite on colorectal cancer cell lines. Kanglaite pretreatment followed by Taxol treatment was found to show the best synergism among all combination strategies. This combination also resulted in the smallest tumour volume in a Balb/c mice model. Kanglaite inhibited the expression of nuclear factor (NF)-κΒ and upregulated that of connexin 43, both of which sensitized cancer cells to Taxol. Moreover, Kanglaite increased many cellular variations caused by Taxol, including tubulin polymerization, caspase-3 cleavage, and upregulated expression of survivin and cyclin B1. These results suggest that Kanglaite pretreatment may increase the effect of Taxol on colorectal cancer.
“…In addition, KLT pretreatment enhanced the upregulation of survivin expression caused by Taxol, and the “KLT+Taxol” group had the highest survivin expression. These results are consistent with those reported in other studies 27, 28 .Figure 4Western blotting results of cyclin B1, survivin, Cx43, caspase-3, PARP and caspase-8 in four colorectal cancer cell lines, HCT106, HCT116, LoVo, and CT26, which were treated with different combinations of drugs. β-Actin or GAPDH was used as a loading control.…”
Taxol, a first-line anti-tumour drug, has low effectiveness against colorectal cancer. Combination with other agents is an effective strategy to enhance Taxol cytotoxicity. Kanglaite injection is an extract from Coix lacryma-jobi seed and is usually combined with other agents to treat cancer. The aim of this study was to investigate the treatment effect of Taxol combined with Kanglaite on colorectal cancer cell lines. Kanglaite pretreatment followed by Taxol treatment was found to show the best synergism among all combination strategies. This combination also resulted in the smallest tumour volume in a Balb/c mice model. Kanglaite inhibited the expression of nuclear factor (NF)-κΒ and upregulated that of connexin 43, both of which sensitized cancer cells to Taxol. Moreover, Kanglaite increased many cellular variations caused by Taxol, including tubulin polymerization, caspase-3 cleavage, and upregulated expression of survivin and cyclin B1. These results suggest that Kanglaite pretreatment may increase the effect of Taxol on colorectal cancer.
“…NLK was presumed to be a tumor suppressor gene in ovarian cancer, glioma and prostate cancer [22–24]. While in gallbladder cancer, hepatocellular carcinoma and laryngeal cancer, NLK functioned as oncogene [25–27]. In a recent study, the expression levels of NLK were significantly upregulated in CRC tissues compared to which in matched non-tumor tissues, and the NLK expression was significantly correlated with the clinicopathological features including the depth of tumor invasion [28].…”
BackgroundMicroRNAs play an ess
ential role in colorectal cancer development and progression. Aberrant miR-409-3p expression has been reported in several cancers. However, the clinical significance and functions of miR-409-3p in human CRC were not entirely clear.MethodsmiR-409-3p expression levels were determined in 45 pairs of primary CRC and their corresponding adjacent non-tumor tissues by qPCR. The effects of ectopic expression of miR-409-3p on CRC cells proliferation, wound healing, metastasis were investigated by CCK-8, transwell assay and peritoneal spreading nude mice model.ResultsStatistical analysis of clinical cases revealed that low miR-409-3p expression had inclinations towards lager tumor size and local invasion. Ectopic expression of miRNA mimics suggested that miR-409-3p could inhibits the abilities of proliferation, wound healing, metastasis and invasion in CRC cells. Notably, we found the NLK could be a potential target of miR-409-3p.ConclusionOur results suggest that miR-409-3p functions as a tumor suppressor by inhibiting the development and metastasis of CRC, suggesting that miR-409-3p is expected to become a new diagnostic marker and a new target of the treatment of CRC.
“…Cell proliferation is inhibited when NLK is downregulated in Hep-2 cells via transfection of lentivirus-mediated RNAi (LV-shNLK), and cell numbers of the LV-shNLK treated with Taxol group are less than those in the LV-shcontrol+Taxol group. FCM analysis indicates that Lv-shNLK+Taxol causes the G0/G1 phase DNA content to decrease from 44.1 to 3.33 % and the S phase DNA content to increase from 38.4 to 82.0 % compared with the Lv-shcontrol+Taxol group [22].…”
Nemo-like kinase (NLK) is an evolutionarily conserved mitogen-activated protein (MAP) kinase-related kinase that is highly expressed in neural tissues and minimally detected in others. Accumulating evidence demonstrates that NLK exerts a pivotal role in cell proliferation, migration, invasion, and apoptosis via regulation of a variety of transcriptional molecules. The results of recent studies have shown that aberrant expression of NLK is significantly associated with the initiation and progression of various types of human cancers, as well as clinicopathologic features and survival rate. NLK is gradually considered as a potential tumor suppressor or an oncogene depending on the tumor system, and silencing or upregulating of NLK may provide an effective therapeutic approach against tumors. In this review, we will make a summary on the comprehensive roles of NLK in the regulation of various cancers.
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