Dual-Specificity Phosphatase 4 Promotes Malignant Features in Colorectal Cancer Through Cyclic-AMP Response Element Binding Protein/Protein Kinase CAMP-Activated Catalytic Subunit Beta Activation.

Apoptosis Colorectal cancer DUSP4 Migration PRKACB/CREB Proliferation

Journal

Digestive diseases and sciences
ISSN: 1573-2568
Titre abrégé: Dig Dis Sci
Pays: United States
ID NLM: 7902782

Informations de publication

Date de publication:
01 Jun 2024
Historique:
received: 09 11 2023
accepted: 06 05 2024
medline: 2 6 2024
pubmed: 2 6 2024
entrez: 1 6 2024
Statut: aheadofprint

Résumé

Previous studies have demonstrated that Dual-specificity phosphatase 4 (DUSP4) plays an important role in the progression of different tumor types. However, the role and mechanism of DUSP4 in colorectal cancer (CRC) remain unclear. We investigate the role and mechanisms of DUSP4 in CRC. Immunohistochemistry was used to investigate DUSP4 expression in CRC tissues. Cell proliferation, apoptosis and migration assays were used to validate DUSP4 function in vitro and in vivo. RNA-sequence assay was used to identify the target genes of DUSP4. Human phosphokinase array and inhibitor assays were used to explore the downstream signaling of DUSP4. DUSP4 expression was upregulated in CRC tissues relative to normal colorectal tissues, and DUSP4 expression showed a significant positive correlation with CRC stage. Consistently, we found that DUSP4 was highly expressed in colorectal cancer cells compared to normal cells. DUSP4 knockdown inhibits CRC cell proliferation, migration and promotes apoptosis. Furthermore, the ectopic expression of DUSP4 enhanced CRC cell proliferation, migration and diminished apoptosis in vitro and in vivo. Human phosphokinase array data showed that ectopic expression of DUSP4 promotes CREB activation. RNA-sequencing data showed that PRKACB acts as a downstream target gene of DUSP4/CREB and enhances CREB activation through PKA/cAMP signaling. In addition, xenograft model results demonstrated that DUSP4 promotes colorectal tumor progression via PRKACB/CREB activation in vivo. These findings suggest that DUSP4 promotes CRC progression. Therefore, it may be a promising therapeutic target for CRC.

Identifiants

pubmed: 38824257
doi: 10.1007/s10620-024-08481-y
pii: 10.1007/s10620-024-08481-y
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Fundamental Scientific Research Project of Tianjin University of China
ID : 2017KJ191

Informations de copyright

© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

Références

Dekker E, Tanis PJ, Vleugels JLA, Kasi PM, Wallace MB. Colorectal cancer. Lancet (Lond, Engl). 2019;394:1467–1480.
doi: 10.1016/S0140-6736(19)32319-0
Siegel RL, Giaquinto AN. Cancer statistics. J CA 2024;2024:12–49.
Cai M, Gao Z, Liao J, Jiang Y, He Y. Frailty affects prognosis in patients with colorectal cancer: A systematic review and meta-analysis. Front Oncol. 2022;12:1017183.
pubmed: 36408138 pmcid: 9669723 doi: 10.3389/fonc.2022.1017183
Yip-Schneider MT, Lin A, Marshall MS. Pancreatic tumor cells with mutant K-ras suppress ERK activity by MEK-dependent induction of MAP kinase phosphatase-2. Biochem Biophys Res Commun. 2001;280:992–997.
pubmed: 11162624 doi: 10.1006/bbrc.2001.4243
Hu B, Zhang D, Zhao K et al. Spotlight on USP4: structure, function, and regulation. Front Cell Dev Biol. 2021;9:595159.
pubmed: 33681193 pmcid: 7935551 doi: 10.3389/fcell.2021.595159
Lawan A, Torrance E, Al-Harthi S et al. MKP-2: out of the DUSP-bin and back into the limelight. Biochem Soc Trans 2012;40:235–239.
pubmed: 22260697 doi: 10.1042/BST20110648
Jeong DG, Jung SK, Yoon TS et al. Crystal structure of the catalytic domain of human MKP-2 reveals a 24-mer assembly. Proteins. 2009;76:763–767.
pubmed: 19415758 doi: 10.1002/prot.22423
Zhang T, Mulvaney JM, Roberson MS. Activation of mitogen-activated protein kinase phosphatase 2 by gonadotropin-releasing hormone. Mol Cell Endocrinol 2001;172:79–89.
pubmed: 11165042 doi: 10.1016/S0303-7207(00)00378-6
Bignon A, Régent A, Klipfel L et al. DUSP4-mediated accelerated T-cell senescence in idiopathic CD4 lymphopenia. Blood. 2015;125:2507–2518.
pubmed: 25733583 doi: 10.1182/blood-2014-08-598565
Tresini M, Lorenzini A, Torres C, Cristofalo VJ. Modulation of replicative senescence of diploid human cells by nuclear ERK signaling. J Biol Chem. 2007;282:4136–4151.
pubmed: 17145763 doi: 10.1074/jbc.M604955200
Cadalbert L, Sloss CM, Cameron P, Plevin R. Conditional expression of MAP kinase phosphatase-2 protects against genotoxic stress-induced apoptosis by binding and selective dephosphorylation of nuclear activated c-jun N-terminal kinase. Cell Signal. 2005;17:1254–1264.
pubmed: 16038800 doi: 10.1016/j.cellsig.2005.01.003
Huang S, Ma Z, Zhou Q et al. Genome-wide CRISPR/Cas9 library screening identified that DUSP4 deficiency induces lenvatinib resistance in hepatocellular carcinoma. Int J Biol Sci. 2022;18:4357–4371.
pubmed: 35864956 pmcid: 9295068 doi: 10.7150/ijbs.69969
Hanna A, Nixon MJ, Estrada MV et al. Combined Dusp4 and p53 loss with Dbf4 amplification drives tumorigenesis via cell cycle restriction and replication stress escape in breast cancer. Breast Cancer Res. 2022;24:51.
pubmed: 35850776 pmcid: 9290202 doi: 10.1186/s13058-022-01542-y
Zeng X, Zhu C, Zhu X. DUSP4 promotes the carcinogenesis of CCRCC via negative regulation of autophagic death. Biosci Biotechnol Biochem. 2021;85:1839–1845.
pubmed: 34143206 doi: 10.1093/bbb/zbab111
Chesnokov MS, Yadav A, Chefetz I. Optimized transcriptional signature for evaluation of MEK/ERK pathway baseline activity and long-term modulations in ovarian cancer. Int J Mol Sci. 2022;23:8.
doi: 10.3390/ijms232113365
Sieben NL, Oosting J, Flanagan AM et al. Differential gene expression in ovarian tumors reveals Dusp 4 and Serpina 5 as key regulators for benign behavior of serous borderline tumors. J Clin Oncol. 2005;23:7257–7264.
pubmed: 16087957 doi: 10.1200/JCO.2005.02.2541
Wu W, Wei H, Hu S et al. Long noncoding RNA PCAT6 regulates cell proliferation and migration in human esophageal squamous cell carcinoma. J Cancer. 2022;13:681–690.
pubmed: 35069911 pmcid: 8771521 doi: 10.7150/jca.62671
Han J, Ye S, Chen J et al. Lysine-specific histone demethylase 1 promotes oncogenesis of the esophageal squamous cell carcinoma by upregulating DUSP4. Biochem Biokhimiia. 2021;86:1624–1634.
doi: 10.1134/S0006297921120117
Hijiya N, Tsukamoto Y, Nakada C et al. Genomic loss of DUSP4 contributes to the progression of intraepithelial neoplasm of pancreas to invasive carcinoma. Cancer Res. 2016;76:2612–2625.
pubmed: 26941286 doi: 10.1158/0008-5472.CAN-15-1846
Al-Mutairi MS, Habashy HO. DUSP4 silencing enhances the sensitivity of breast cancer cells to doxorubicin through the activation of the JNK/c-Jun signalling pathway. Molecules (Basel, Switzerland). 2022;27:89.
doi: 10.3390/molecules27196146
Chen M, Zhang J, Berger AH et al. Compound haploinsufficiency of Dok2 and Dusp4 promotes lung tumorigenesis. J Clin Invest. 2019;129:215–222.
pubmed: 30475228 doi: 10.1172/JCI99699
Lin H, Qiu S, Xie L, Liu C, Sun S. Nimbolide suppresses non-small cell lung cancer cell invasion and migration via manipulation of DUSP4 expression and ERK1/2 signaling. Biomed Pharmacother. 2017;92:340–346.
pubmed: 28554129 doi: 10.1016/j.biopha.2017.05.072
Xue Z, Vis DJ, Bruna A et al. MAP3K1 and MAP2K4 mutations are associated with sensitivity to MEK inhibitors in multiple cancer models. Cell Res. 2018;28:719–729.
pubmed: 29795445 pmcid: 6028652 doi: 10.1038/s41422-018-0044-4
Kwok RP, Lundblad JR, Chrivia JC et al. Nuclear protein CBP is a coactivator for the transcription factor CREB. Nature. 1994;370:223–226.
pubmed: 7913207 doi: 10.1038/370223a0
Wang H, Xu J, Lazarovici P, Quirion R, Zheng W. cAMP Response element-binding protein (CREB): a possible signaling molecule link in the pathophysiology of schizophrenia. Front Mol Neurosc. 2018;11:255.
doi: 10.3389/fnmol.2018.00255
Lu F, Zheng Y, Donkor PO, Zou P, Mu P. Downregulation of CREB promotes cell proliferation by mediating G1/S phase transition in hodgkin lymphoma. Oncol Res. 2016;24:171–179.
pubmed: 27458098 pmcid: 7838744 doi: 10.3727/096504016X14634208142987
Sandoval S, Pigazzi M, Sakamoto KM. CREB: A key regulator of normal and neoplastic hematopoiesis. Adv Hematol. 2009;2009:634292.
pubmed: 19960054 pmcid: 2778441 doi: 10.1155/2009/634292
Li J, Liu X, Wang W, Li C, Li X. MSK1 promotes cell proliferation and metastasis in uveal melanoma by phosphorylating CREB. Archiv Med Sci. 2020;16:1176–1188.
doi: 10.5114/aoms.2019.85810
Meng XY, Zhang HZ, Ren YY et al. Pinin promotes tumor progression via activating CREB through PI3K/AKT and ERK/MAPK pathway in prostate cancer. Am J Cancer Res. 2021;11:1286–1303.
pubmed: 33948358 pmcid: 8085840
Bolger GB. The cAMP-signaling cancers: Clinically-divergent disorders with a common central pathway. Front Endocrinol. 2022;13:1024423.
doi: 10.3389/fendo.2022.1024423
Taylor SS, Wallbott M, Machal EMF et al. PKA Cβ: a forgotten catalytic subunit of cAMP-dependent protein kinase opens new windows for PKA signaling and disease pathologies. Biochem J. 2021;478:2101–2119.
pubmed: 34115095 doi: 10.1042/BCJ20200867
Evan GI, Vousden KH. Proliferation, cell cycle and apoptosis in cancer. Nature. 2001;411:342–348.
pubmed: 11357141 doi: 10.1038/35077213
Yao X, Hu W, Zhang J, Huang C, Zhao H, Yao X. Application of cAMP-dependent catalytic subunit β (PRKACB) low expression in predicting worse overall survival: a potential therapeutic target for colorectal carcinoma. J Cancer. 2020;11:4841–4850.
pubmed: 32626531 pmcid: 7330678 doi: 10.7150/jca.46156
Shen W, Du W, Li Y et al. TIFA promotes colorectal cancer cell proliferation in an RSK- and PRAS40-dependent manner. Cancer Sci. 2022;113:3018–3031.
pubmed: 35635239 pmcid: 9459298 doi: 10.1111/cas.15432
Shen W, Xie J, Zhao S et al. ICAM3 mediates inflammatory signaling to promote cancer cell stemness. Cancer Lett. 2018;422:29–43.
pubmed: 29477378 pmcid: 5928798 doi: 10.1016/j.canlet.2018.02.034
Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144:646–674.
pubmed: 21376230 doi: 10.1016/j.cell.2011.02.013
Patterson KI, Brummer T, O’Brien PM, Daly RJ. Dual-specificity phosphatases: critical regulators with diverse cellular targets. Biochem J. 2009;418:475–489.
pubmed: 19228121 doi: 10.1042/BJ20082234
Ito T, Young MJ, Li R et al. Paralog knockout profiling identifies DUSP4 and DUSP6 as a digenic dependence in MAPK pathway-driven cancers. Nat Genet. 2021;53:1664–1672.
pubmed: 34857952 doi: 10.1038/s41588-021-00967-z
Xu W, Chen B, Ke D, Chen X. DUSP4 directly deubiquitinates and stabilizes Smad4 protein, promoting proliferation and metastasis of colorectal cancer cells. Aging (Albany NY). 2020;12:17634–17646.
pubmed: 32897241 pmcid: 7521518 doi: 10.18632/aging.103823
Ichimanda M, Hijiya N, Tsukamoto Y et al. Downregulation of dual-specificity phosphatase 4 enhances cell proliferation and invasiveness in colorectal carcinomas. Cancer Sci. 2018;109:250–258.
pubmed: 29150975 doi: 10.1111/cas.13444
Zhang H, Kong Q, Wang J, Jiang Y, Hua H. Complex roles of cAMP-PKA-CREB signaling in cancer. Exp Hematol Oncol. 2020;9:32.
pubmed: 33292604 pmcid: 7684908 doi: 10.1186/s40164-020-00191-1
Wong JC, Bathina M, Fiscus RR. Cyclic GMP/protein kinase G type-Iα (PKG-Iα) signaling pathway promotes CREB phosphorylation and maintains higher c-IAP1, livin, survivin, and Mcl-1 expression and the inhibition of PKG-Iα kinase activity synergizes with cisplatin in non-small cell lung cancer cells. J Cell Biochem. 2012;113:3587–3598.
pubmed: 22740515 doi: 10.1002/jcb.24237

Auteurs

Wenju Pei (W)

Department of General Surgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Department of General Surgery, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, 272067, China.
Key Laboratory of Precision Oncology in Universities of Shandong, Institute of Precision Medicine, Jining Medical University, Jining, 272067, China.

Wanbin Yin (W)

Department of General Surgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Department of General Surgery, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, 272067, China.

Tao Yu (T)

Department of Medical Oncology, Tianjin Medical University General Hospital, Tianjin, 300052, China.

Xiaoyuan Zhang (X)

Key Laboratory of Precision Oncology in Universities of Shandong, Institute of Precision Medicine, Jining Medical University, Jining, 272067, China.

Qi Zhang (Q)

Department of General Surgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.

Xiaowen Yang (X)

Key Laboratory of Precision Oncology in Universities of Shandong, Institute of Precision Medicine, Jining Medical University, Jining, 272067, China.

Chunlei Shi (C)

Department of General Surgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.

Wenzhi Shen (W)

Key Laboratory of Precision Oncology in Universities of Shandong, Institute of Precision Medicine, Jining Medical University, Jining, 272067, China. shenwenzhi2011@126.com.

Gang Liu (G)

Department of General Surgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.

Classifications MeSH