Lentivirus-based RNA Silencing of Nemo-like Kinase (NLK) Inhibits the CAL 27 Human Adenosquamos Carcinoma Cells Proliferation and Blocks G0/G1 Phase to S Phase

Zhang, Bin; Li, Ke Yi; Chen, Hai-Ying; Chen, Shuang Feng; Zhang, Wei Feng; Xia, Chun Peng; Jiang, Li; Liu, Xian Bin; Zhao, Feng; Yuan, Dao Ying; Wang, Le Xin; Wu, Ya Ping; Liu, Shu Wei

doi:10.7150/ijms.6607

Cited by 7 publications

(5 citation statements)

References 18 publications

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“…On the other hand, NLK also appears to function as an oncogene in some cancers, including oral adenosquamous carcinoma [22], nasopharyngeal carcinoma [23], gallbladder cancer [10], and HCC [12]. In the human oral adenosquamous carcinoma cells, targeted disruption of NLK could significantly inhibit the proliferation and colony formation ability of CAL-27 cells [22].…”

Section: Discussionmentioning

confidence: 98%

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Prognostic significance of Nemo-like kinase expression in patients with hepatocellular carcinoma

Chen

Qiao

et al. 2015

Tumor Biol.

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Nemo-like kinase (NLK) is an evolutionarily conserved serine/threonine protein kinase and belongs to the extracellular signal-regulated kinases/microtubule-associated protein kinase families (Erks/MAPKs). Previous studies have indicated that abnormal expressions of NLK played critical roles in various types of human cancers. Recent studies suggested that NLK expression was significantly upregulated in the hepatocellular carcinoma (HCC) specimens. However, the clinical significance of NLK expression in HCC remains largely unknown. In this study, we focused on the clinical significance of NLK in HCC and found that high expression of NLK was significantly associated with Edmondson-Steiner grade (P = 0.002), tumor size (P = 0.022), and no. of tumor nodules (P < 0.001), and NLK was positively correlated with proliferation marker Ki-67 (P < 0.01). Univariate analysis suggested that NLK expression was associated with poor prognosis (P < 0.001). Multivariate analysis indicated that NLK expression was an independent prognostic indicator for HCC (P = 0.0370). In conclusion, NLK overexpression is associated with poor overall survival in patients with HCC, it might be an independent poor prognostic marker for HCC.

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Section: Discussionmentioning

confidence: 98%

“…In the human oral adenosquamous carcinoma cells, targeted disruption of NLK could significantly inhibit the proliferation and colony formation ability of CAL-27 cells [22]. In nasopharyngeal carcinoma (NPC), NLK positivity was associated with tumor extent, regional lymph node status, and distant metastases [23].…”

Section: Discussionmentioning

confidence: 99%

Prognostic significance of Nemo-like kinase expression in patients with hepatocellular carcinoma

Chen

Qiao

et al. 2015

Tumor Biol.

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“…Notably, microRNA-125b arrested the cell cycle at the G1 to S transition to prevent cell proliferation and metastasis in human liver cancer (14). Nemo-like kinase expression knockdown blocks the G0/G1 phase to S phase transition to inhibit human adenosquamous carcinoma cells CAL-27 proliferation and colony formation (15). During the present study, knockdown of RTN4 caused a decrease in the percentage of cells in S phase and G2/M phase, but resulted in an increase of cells in G0/G1 phase, in particular there was an increased number of apoptotic cells, as indicated by an increase of cells in sub-G1 phase, which suggests that RTN4-C may regulate G0/G1 to S phase transition and inhibit cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of reticulon 4C by lentivirus inhibits human colorectal cancer cell growth

Xue

Wang

Chen

et al. 2015

Molecular Medicine Reports

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Colorectal cancer is the third most common type of cancer worldwide with high cell motility and metastatic potential. Reticulon 4C (RTN4-C) is the shortest isoform of the reticulon family protein RTN4, which may act to induce cell apoptosis and suppress tumor development. The aim of the present study was to determine the role of RTN4-C in colorectal cancer, and potentially identify a novel target for anti-tumor therapy. To investigate the biological role of RTN4-C in colorectal cancer, the expression levels of RTN4-C were initially analyzed in six colorectal cancer cell lines by reverse transcription-quantitative polymerase chain reaction and western blot analysis. In addition, lentivirus-based RNA interference was utilized to knock down RTN4-C expression in RKO and DLD-1 cells with low and high levels of RTN4-C, respectively. The rate of proliferation decreased in RTN4-C silenced RKO and DLD-1 cells compared with the control, as determined using MTT and colony formation assays. Flow cytometric analysis revealed that RTN4-C knockdown in RKO cells led to cell cycle arrest at the G0/G1 phase, particularly at the sub-G1 phase representing apoptotic cells. These results indicate that RTN4-C has an important role in colorectal cancer cell growth, which may provide a potential therapeutic approach for human colorectal cancer.

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“…In contrast, it was found to negatively regulate the ternary transcriptional complex in the Notch signaling pathway that is crucial in cell fates of metazoan tissues [ 65 ]. Aberrant expression of NLK has been associated with the initiation or progression of oral squamous cell carcinoma [ 66 ], laryngeal cancer [ 67 ], non-small-cell lung cancer (NSCLC) [ 68 , 69 ], and CRC [ 70 ]. The CAMKK1 gene mediated the upstream activation of AMP-activated protein kinase (AMPK) by phosphorylation of the α-subunit threonine 172 (Thr172) residue.…”

Section: Discussionmentioning

confidence: 99%

Identification of Differentially Methylated CpG Sites in Fibroblasts from Keloid Scars

et al. 2020

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As a part of an abnormal healing process of dermal injuries and irritation, keloid scars arise on the skin as benign fibroproliferative tumors. Although the etiology of keloid scarring remains unsettled, considerable recent evidence suggested that keloidogenesis may be driven by epigenetic changes, particularly, DNA methylation. Therefore, genome-wide scanning of methylated cytosine-phosphoguanine (CpG) sites in extracted DNA from 12 keloid scar fibroblasts (KF) and 12 control skin fibroblasts (CF) (six normal skin fibroblasts and six normotrophic fibroblasts) was conducted using the Illumina Human Methylation 450K BeadChip in two replicates for each sample. Comparing KF and CF used a Linear Models for Microarray Data (Limma) model revealed 100,000 differentially methylated (DM) CpG sites, 20,695 of which were found to be hypomethylated and 79,305 were hypermethylated. The top DM CpG sites were associated with TNKS2, FAM45B, LOC723972, GAS7, RHBDD2 and CAMKK1. Subsequently, the most functionally enriched genes with the top 100 DM CpG sites were significantly (p ≤ 0.05) associated with SH2 domain binding, regulation of transcription, DNA-templated, nucleus, positive regulation of protein targeting to mitochondrion, nucleoplasm, Swr1 complex, histone exchange, and cellular response to organic substance. In addition, NLK, CAMKK1, LPAR2, CASP1, and NHS showed to be the most common regulators in the signaling network analysis. Taken together, these findings shed light on the methylation status of keloids that could be implicated in the underlying mechanism of keloid scars formation and remission.

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Lentivirus-based RNA Silencing of Nemo-like Kinase (NLK) Inhibits the CAL 27 Human Adenosquamos Carcinoma Cells Proliferation and Blocks G0/G1 Phase to S Phase

Cited by 7 publications

References 18 publications

Prognostic significance of Nemo-like kinase expression in patients with hepatocellular carcinoma

Prognostic significance of Nemo-like kinase expression in patients with hepatocellular carcinoma

Knockdown of reticulon 4C by lentivirus inhibits human colorectal cancer cell growth

Identification of Differentially Methylated CpG Sites in Fibroblasts from Keloid Scars

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