LACTB promotes metastasis of nasopharyngeal carcinoma via activation of ERBB3/EGFR-ERK signaling resulting in unfavorable patient survival

Peng, Li‐Xia; Wang, Ming‐Dian; Xie, Ping; Yang, Junping; Sun, Rui; Zheng, Lixin; Yan, Mei; Meng, Dongfang; Peng, Xing-Si; Lang, Yan-Hong; Qiang, Ya‐Wei; Li, Chang‐Zhi; Xu, Liang; Liu, Zhijie; Guo, Lingling; Xie, Donglai; Shu, Ditian; Lin, Shi; Luo, Fengming; Huang, Bi‐Jun; Qian, Chao‐Nan

doi:10.1016/j.canlet.2020.10.051

Cited by 22 publications

(23 citation statements)

References 52 publications

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“…Zeng et al demonstrated that LACTB attenuated p53 ubiquitination and inhibited the progression of colorectal cancer (10). However, in contrast, LACTB was found to contribute to cancer metastasis and to correlate with the poor prognosis of nasopharyngeal and pancreatic cancer (11,12). These data suggest that the role of LACTB differs in a particular cancer.…”

Section: Lactb Suppresses Carcinogenesis In Lung Cancer and Regulates...mentioning

confidence: 99%

LACTB suppresses carcinogenesis in lung cancer and regulates the EMT pathway

Shi

Wang

et al. 2022

Exp Ther Med

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Lung cancer causes thousands of deaths worldwide every year, and present therapeutics show little benefit for advanced-stage patients. Researchers do not know why and how lung cancer begins. Lactamase β (LACTB) is a tumor-suppressor in some cancers. However, its role in lung cancer is unknown. By analyzing the TCGA database and Kaplan-Meier Plotter database, LACTB was found to be downregulated in lung cancer tissues but the methylation level was increased. Patients with high LACTB expression exhibited improved survival. Then, in vitro assays demonstrated that LACTB overexpression inhibited cell migration and invasion, and induced apoptosis in H1299 and H1975 cells. Knockdown of LACTB caused the reverse effects. Moreover, a much higher apoptotic rate and more potent inhibitory effects on H1299 and H1975 cells were obtained when LACTB was combined with docetaxel. In addition, members of the epithelial-mesenchymal transition (EMT) signaling pathway were assessed using western blot analysis. The expression of E-cadherin was decreased while levels of N-cadherin and vimentin were increased after knockdown of LACTB in lung cancer cells. By contrast, overexpression of LACTB increased the level of E-cadherin but decreased N-cadherin and vimentin. Therefore, LACTB is a tumor suppressor in lung cancer that inhibits cell migration and invasion and induces cell apoptosis. Meanwhile, LACTB was found to strengthen the anticancer role of docetaxel and to suppress the EMT pathway in lung cancer.

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Section: Lactb Suppresses Carcinogenesis In Lung Cancer and Regulates...mentioning

confidence: 99%

LACTB suppresses carcinogenesis in lung cancer and regulates the EMT pathway

Shi

Wang

et al. 2022

Exp Ther Med

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“…In addition, LACTB dysregulation in melanoma, gastric cancer, glioma cancer, and colorectal cancer patients can serve as a marker for tumor development and prognosis (Jiang et al, 2020;Li et al, 2019;Ma et al, 2021;Wang et al, 2020;Xu et al, 2020;Yang et al, 2021aYang et al, , 2021bZeng et al, 2018). Moreover, LACTB overexpression has been shown to contribute to several cancers, including nasopharyngeal carcinoma and pancreatic adenocarcinoma (Peng et al, 2021;Xie et al, 2021). Although many diseases have associated abnormalities in LACTB expression or function, the underlying mechanism remains unclear due to a lack of structural analyses.…”

Section: Introductionmentioning

confidence: 99%

Structural basis for the catalytic activity of filamentous human serine beta-lactamase-like protein LACTB

Zhang

Guo

et al. 2022

Structure

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“…Distant metastasis has become one of the main causes of treatment failure in cancer patients [ 6 ]. Once NPC patients develop distant metastases, the overall prognosis is poor and the cure rate is low [ 7 ]. Distant metastases are common in bone, lung, liver, and distant lymph nodes, most of which occur within 3 years after radical radiotherapy.…”

Section: Introductionmentioning

confidence: 99%

Differentially Expressed Genes in Nasopharyngeal Carcinoma Tissues and Their Correlation with Recurrence and Metastasis of Nasopharyngeal Carcinoma

Yue

Zhu

Luo

et al. 2022

Computational and Mathematical Methods in Medicine

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In this study, bioinformatics tools were used to identify key genes to study the molecular mechanism of nasopharyngeal carcinoma (NPC) development and to explore the correlation of these key genes with the recurrence and metastasis of NPC. The GSE61218 microarray dataset obtained from the Gene Expression Omnibus Database (GEO) was used. The limma R package was used to screen differentially expressed genes (DEGs) between NPC and normal nasopharyngeal (NP) tissues. KEGG functional enrichment was performed on these selected DEGs. Protein-protein interaction (PPI) networks were constructed using Cytoscape software to identify key node proteins. The NPC-metastasis microarray dataset GSE103611 was obtained from GEO to analyze the expression of DEGs in NPC metastasis. A total of 239 DEGs were identified. DEGs were mainly enriched in oocyte maturation-related pathways, cytokine-related pathways, cell cycle-related pathways, cancer-related pathways, and homologous recombination-related pathways. In addition, the top 10 nodes with the higher degree in the DEG PPI network were as follows: CDK1, CCNB2, BUB1, CCNA2, AURKB, BUB1B, MAD2L1, NDC80, BIRC5, and CENPF. The results indicated that DEGs may be involved in the pathogenesis of NPC by regulating cell cycle and mitosis, which can be used as molecular biomarkers for the diagnosis of NPC. In addition, we identified 87 DEGs with FC > 2 and P < 0.01 from the metastasis spectrum of NPC. The intersection gene between DEGs of NPC and normal NP tissue samples and those of the metastatic spectrum of NPC was identified to be VRK2. The expression of VRK2 in NPC samples was significantly higher than that in normal NP tissue, and similarly, VRK2 expression was significantly upregulated in metastatic samples compared with nonmetastatic samples ( P < 0.05 ). Therefore, VRK2 may be a biomarker for predicting the metastasis of NPC patients after treatment.

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LACTB promotes metastasis of nasopharyngeal carcinoma via activation of ERBB3/EGFR-ERK signaling resulting in unfavorable patient survival

Cited by 22 publications

References 52 publications

LACTB suppresses carcinogenesis in lung cancer and regulates the EMT pathway

LACTB suppresses carcinogenesis in lung cancer and regulates the EMT pathway

Structural basis for the catalytic activity of filamentous human serine beta-lactamase-like protein LACTB

Differentially Expressed Genes in Nasopharyngeal Carcinoma Tissues and Their Correlation with Recurrence and Metastasis of Nasopharyngeal Carcinoma

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