Over‐expression of USP15/MMP3 predict poor prognosis and promote growth, migration in non-small cell lung cancer cells

Chen, Weiwei; Ni, Daguang; Zhang, Hailin; Li, Xia; Jiang, Yinghua; Wu, Jixiang; Gu, Yan; Gao, Mingcheng; Shi, Woda; Song, Jianxiang; Shi, Wenyu

doi:10.1016/j.cancergen.2023.01.001

Cited by 8 publications

(5 citation statements)

References 34 publications

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“…Within cellular pathways crucial for cell proliferation, development, and innate immunity, USP15 assumes a substantial role [31,32]. Its involvement in cancer progression, including lung cancer, has been welldocumented [33,34]. Furthermore, USP15 has shown upregulation in various other cancer types, such as glioblastoma, breast cancer, ovarian cancer and gastric cancer, to name a few [35][36][37].…”

Section: Discussionmentioning

confidence: 99%

USP15 facilitates the progression of bladder cancer by amplifying the activation of the NF-κB signaling pathway

Li,

Jiang,

Liu

et al. 2024

Aging

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USP15, a pivotal member of the deubiquitinase family, plays a crucial role in orchestrating numerous vital biological processes, including the regulation of NF-κB signaling pathway and deubiquitination of protooncogenes. In various cancers, USP15 has been validated to exhibit up-regulated expression, impacting the initiation and progression of cancer. However, its precise mechanism in bladder cancer remains elusive. Our study shed light on the significant overexpression of USP15 in bladder cancer cells compared to normal bladder cells, correlating with a poorer prognosis for bladder cancer patients. Strikingly, attenuation of USP15 expression greatly attenuated the proliferation, migration, and invasion of bladder cancer cells. Moreover, upregulation of USP15 was found to drive cancer progression through the activation of the NF-κB signaling pathway. Notably, USP15 directly deubiquitinates BRCC3, heightening its expression level, and subsequent overexpression of BRCC3 counteracted the antitumoral efficacy of USP15 downregulation. Overall, our findings elucidated the carcinogenic effects of USP15 in bladder cancer, primarily mediated by the excessive activation of the NF-κB signaling pathway, thereby promoting tumor development. These results underscore the potential of USP15 as a promising therapeutic target for bladder cancer in the future.

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Section: Discussionmentioning

confidence: 99%

USP15 facilitates the progression of bladder cancer by amplifying the activation of the NF-κB signaling pathway

Li,

Jiang,

Liu

et al. 2024

Aging

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“…Lung adenocarcinoma is a type of non-small cell lung cancer (NSCLC), most of which originate from bronchial mucosal epithelium. 9 The disease progresses slowly; hence, the initial symptoms are generally not evident. Most of the patients have already contacted the advanced stage at the time of diagnosis, and it is difficult to have good results through traditional treatment methods, such as surgery and chemoradiotherapy (CRT, CRTx, CT-RT).…”

Section: Discussionmentioning

confidence: 99%

RNF135 promotes cell proliferation and autophagy in lung adenocarcinoma by promoting the phosphorylation of ULK1

Zhuang,

Shi,

Sun

2024

Allergol Immunopathol

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Objective: To detect the expression of RING finger protein 135 (RNF135) in lung adenocarcinoma tissues and explore its role in the progression of lung adenocarcinoma. Methods: Bioinformation analysis, quantitative polymerase chain reaction, and immunoblotting technique discovered the expression of RNF135 in lung adenocarcinoma tissues. Cell counting kit-8 and colony formation, immunostaining, and immunoblot assays examined the effects of RNF135 on cell growth and autophagy. Co-immunoprecipitation (Co-IP), immunostaining, and immuoblotting were conducted to confirm the mechanism. Results: RNF135 was highly expressed in lung adenocarcinoma. In addition, RNF135 promoted lung adenocarcinoma cell growth. Further, data confirmed that RNF135 promoted autophagy in lung adenocarcinoma cells. Mechanically, RNF135 directly interacted with Unc-51-like autophagy activating kinase 1 (ULK1) to promote its phosphorylation level. Conclusion: RNF135 promoted cell growth and autophagy in lung adenocarcinoma by promoting the phosphorylation of ULK1.

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“…Moreover, recent research implies that MMP-3 has a role in prostate cancer progression to bone metastasis [ 125 ]. Chen et al have also demonstrated the crucial role of ubiquitin-specific peptidase 15 and MMP3 in non-small-cell lung cancer development and prognosis [ 126 ]. Therefore, MMP-3 is a promising target for the generation of new antineoplastic drugs.…”

Section: Matrix Metalloprotease-3 (Mmp-3)mentioning

confidence: 99%

Matrix Metalloproteinases Inhibitors in Cancer Treatment: An Updated Review (2013–2023)

Almutairi,

Kalloush,

Manoon

et al. 2023

Molecules

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Matrix metalloproteinases (MMPs) are identifiable members of proteolytic enzymes that can degrade a wide range of proteins in the extracellular matrix (ECM). MMPs can be categorized into six groups based on their substrate specificity and structural differences: collagenases, gelatinases, stromelysins, matrilysins, metalloelastase, and membrane-type MMPs. MMPs have been linked to a wide variety of biological processes, such as cell transformation and carcinogenesis. Over time, MMPs have been evaluated for their role in cancer progression, migration, and metastasis. Accordingly, various MMPs have become attractive therapeutic targets for anticancer drug development. The first generations of broad-spectrum MMP inhibitors displayed effective inhibitory activities but failed in clinical trials due to poor selectivity. Thanks to the evolution of X-ray crystallography, NMR analysis, and homology modeling studies, it has been possible to characterize the active sites of various MMPs and, consequently, to develop more selective, second-generation MMP inhibitors. In this review, we summarize the computational and synthesis approaches used in the development of MMP inhibitors and their evaluation as potential anticancer agents.

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Over‐expression of USP15/MMP3 predict poor prognosis and promote growth, migration in non-small cell lung cancer cells

Cited by 8 publications

References 34 publications

USP15 facilitates the progression of bladder cancer by amplifying the activation of the NF-κB signaling pathway

USP15 facilitates the progression of bladder cancer by amplifying the activation of the NF-κB signaling pathway

RNF135 promotes cell proliferation and autophagy in lung adenocarcinoma by promoting the phosphorylation of ULK1

Matrix Metalloproteinases Inhibitors in Cancer Treatment: An Updated Review (2013–2023)

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