NF-κB in pancreatic cancer: Its key role in chemoresistance

Li, Quanxiao; Ye, Gang; Feng, Mengyu; Zheng, Suli; Cao, Zhe; Qiu, Jiangdong; You, Lei; Zheng, Lianfang; Hu, Ya; Zhang, Taiping; Zhao, Yupei

doi:10.1016/j.canlet.2018.02.011

Cited by 83 publications

(69 citation statements)

References 78 publications

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“…Pancreatic cancer is one of the malignant tumors with the worst prognosis. Due to its difficult early diagnosis and treatment, the 5‐year survival rate is less than 1% (Li et al, ; Wang, Baldwin, Nikfarjam, & He, ). Because pancreatic cancer is lack of obvious early symptoms, it is generally diagnosed in the advanced stages (Draper, ; Kitagawa et al, ).…”

Section: Introductionmentioning

confidence: 99%

KIF18B promotes the proliferation of pancreatic ductal adenocarcinoma via activating the expression of CDCA8

Liu

Zhang

et al. 2019

Journal Cellular Physiology

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Pancreatic cancer is one of the malignant tumors with the worst prognosis, and the 5-year survival rate of this disease is less than 1%. About 90% of pancreatic cancer is pancreatic ductal adenocarcinoma (PDAC), and targeting therapy has become a promising treatment for PDAC in recent years. To improve the survival rate, novel therapeutic targets for PDAC are still urgently needed. KIF18B was initially identified as a member of the kinesin family and involved in multiple cellular processes, such as separation of chromosomes in mitosis. Recently, it was found that KIF18B was involved in the growth and development of multiple cancers. However, the potential link between KIF18B and PDAC is still unclear. In this study, we demonstrated that KIF18B was highly expressed in human PDAC tissues, and related with the poor prognosis and clinical features, such as tumor size (*p = .013) and pTNM stage (*p = .025), of patients with PDAC. We further found that KIF18B knockdown blocked the cell proliferation of PDAC in vitro and in vivo, and the cell cycle was arrested caused by KIF18B depletion. Additionally, we also found that KIF18B bound to the promoter region of the cell division cycle associated 8 and thus activated its transcription. Taken together, this study explored the molecular mechanism underlying KIF18B promoting PDAC and provided a novel therapeutic target of this disease. K E Y W O R D SCDCA8, KIF18B, pancreatic ductal adenocarcinoma, proliferation, therapeutic target

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Section: Introductionmentioning

confidence: 99%

KIF18B promotes the proliferation of pancreatic ductal adenocarcinoma via activating the expression of CDCA8

Liu

Zhang

et al. 2019

Journal Cellular Physiology

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“…Moreover, tumor deterioration mainly points to the abnormal changes of NF-κB signal pathway. It has been reported that the abnormal activation of NF-κB signal pathway can accelerate the development of tumors [22], and has an impact on the drug resistance of chemotherapy drugs [23]. The change of NF-κB signaling pathway was consistent with the characteristic of bladder cancer that is easy to relapse and drug resistance.…”

Section: Discussionmentioning

confidence: 57%

The effect of NPM1 silencing on the tumorigenesis of drug-resistant bladder cancer and related signaling pathway

Luo

Lei

Zhao

et al. 2020

Preprint

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Background: NPM1 can provide abundant information of bladder cancer changes, but the effect of NPM1 differential expression on tumor and tumor related molecular mechanism has not been elucidated.Methods: NPM1 silencing cell line was established by lentivirus. The tumorigenic ability was judged by wound-healing assay, transwell invasion assay and nude mice tumorigenicity assay. The proteome of NPM1 deficient bladder cancer cell line was analyzed by Liquid Chromatography Mass Spectrometry (LC-MS). The results of mass spectrometry are comprehensively analyzed by bioinformatics analysis for tumor related molecules. The signal pathways involved in tumor related molecules will be verified by KEGG and UniProt databases.Results: Compared with the corresponding negative control group, NPM1 silencing cell line T24/DDP Lv-NPM1 showed strong migration ability and high invasive ability. There was no significant difference in migration ability and the invasive cells proportion between NPM1 overexpressing cell line and related negative control group. The tumorigenesis in nude mice also showed that NPM1 silencing tumor had larger tumor volume. Among all differential proteins analyzed by mass spectrometry, 20 proteins with signal transduction activity showed the most significant difference (Fold change > 1.5). 6 of them were associated with NF-κB signaling pathway, which may play an important role in the development of tumor.Conclusions: The loss of NPM1 may indicate the poor outcome of bladder cancer. Abnormal expression of NF-κB signaling pathway is an important factor in the progression of bladder cancer. Monitoring NPM1 expression can effectively adjust the treatment strategy of bladder cancer.

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“…TAB2 is an activator of MAP3K7/ TAK1 and is required for TLR-mediated or IL-1-induced NF-kB activation [36,37]. The NF-kB signaling pathway is a key regulator of tumor occurrence and development and can also take part in drug resistance to chemotherapy and targeted therapy [38,39]. Additionally, TAB2 has been reported to serve as a new target for tamoxifen resistance in breast cancer [40], and down-regulation of TAB2 may sensitize NSCLC cells to BMS-690514, a new pan-HER/VEGFR inhibitor [41].…”

Section: Discussionmentioning

confidence: 99%

Analysis of lncRNA, miRNA and mRNA-associated ceRNA networks and identification of potential drug targets for drug-resistant non-small cell lung cancer

Kong¹,

Hu²,

Yuan³

et al. 2020

J. Cancer

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Background: Drug resistance to chemotherapeutic drugs or targeted medicines is an obstacle encountered in the treatment of non-small-cell lung cancer (NSCLC). However, the mechanisms of competing endogenous RNA (ceRNA) on the drug resistance in NSCLC are rarely reported. In this paper, the comprehensive expression profiles of lncRNAs and mRNAs in drug-resistant NSCLC cells were obtained by RNA sequencing. Methods: The dysregulated lncRNAs, miRNAs and mRNAs in drug-resistant NSCLC cell lines were identified by RNA-sequencing and bioinformatics methods. Results: A total of 39 dysregulated lncRNAs and 650 dysregulated mRNAs were identified between drug-resistant NSCLC cell lines and their parental cell lines. Additionally, 33 lncRNA-miRNA-mRNA pathways in the ceRNA network in drug-resistant NSCLC were constructed through bioinformatics methods and ceRNA regulatory rules. These comprised 12 dysregulated lncRNAs, five dysregulated miRNAs, and eight dysregulated mRNAs. In addition, lncRNA ATP2B1/miR-222-5p/TAB2 and lncRNA HUWE1/miR-222-5p/TAB2 were identified as potential ceRNA networks involved in drug resistance to NSCLC. Conclusions: The current study provides a promising therapeutic strategy against the lncRNA-miRNA-mRNA ceRNA regulatory network for NSCLC treatment and deepens our comprehension of the ceRNA regulatory mechanisms related to drug resistance to NSCLC.

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NF-κB in pancreatic cancer: Its key role in chemoresistance

Cited by 83 publications

References 78 publications

KIF18B promotes the proliferation of pancreatic ductal adenocarcinoma via activating the expression of CDCA8

KIF18B promotes the proliferation of pancreatic ductal adenocarcinoma via activating the expression of CDCA8

The effect of NPM1 silencing on the tumorigenesis of drug-resistant bladder cancer and related signaling pathway

Analysis of lncRNA, miRNA and mRNA-associated ceRNA networks and identification of potential drug targets for drug-resistant non-small cell lung cancer

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