NUCKS nuclear elevated expression indicates progression and prognosis of ovarian cancer

Shi, Ce; Qin, Ling; Gao, Hongyu; Gu, Lina; Yang, Chang; Liu, Hebing; Liu, Tianbo

doi:10.1177/1010428317714631

Cited by 14 publications

(10 citation statements)

References 24 publications

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“…Also, the nuclear cyclin-dependent kinase NUCKS was found to be downregulated in HS578T/NOD1. This cell-cycle protein was implicated in tumorigenesis, progression and poor prognosis of several human malignancies [96].…”

Section: Discussionmentioning

confidence: 99%

Proteome profiling of triple negative breast cancer cells overexpressing NOD1 and NOD2 receptors unveils molecular signatures of malignant cell proliferation

et al. 2019

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Background Triple negative breast cancer (TNBC) is a malignancy with very poor prognosis, due to its aggressive clinical characteristics and lack of response to receptor-targeted drug therapy. In TNBC, immune-related pathways are typically upregulated and may be associated with a better prognosis of the disease, encouraging the pursuit for immunotherapeutic options. A number of immune-related molecules have already been associated to the onset and progression of breast cancer, including NOD1 and NOD2, innate immune receptors of bacterial-derived components which activate pro-inflammatory and survival pathways. In the context of TNBC, overexpression of either NOD1 or NOD2 is shown to reduce cell proliferation and increase clonogenic potential in vitro. To further investigate the pathways linking NOD1 and NOD2 signaling to tumorigenesis in TNBC, we undertook a global proteome profiling of TNBC-derived cells ectopically expressing each one of these NOD receptors. Results We have identified a total of 95 and 58 differentially regulated proteins in NOD1 - and NOD2 -overexpressing cells, respectively. We used bioinformatics analyses to identify enriched molecular signatures aiming to integrate the differentially regulated proteins into functional networks. These analyses suggest that overexpression of both NOD1 and NOD2 may disrupt immune-related pathways, particularly NF-κB and MAPK signaling cascades. Moreover, overexpression of either of these receptors may affect several stress response and protein degradation systems, such as autophagy and the ubiquitin-proteasome complex. Interestingly, the levels of several proteins associated to cellular adhesion and migration were also affected in these NOD-overexpressing cells. Conclusions Our proteomic analyses shed new light on the molecular pathways that may be modulating tumorigenesis via NOD1 and NOD2 signaling in TNBC. Up- and downregulation of several proteins associated to inflammation and stress response pathways may promote activation of protein degradation systems, as well as modulate cell-cycle and cellular adhesion proteins. Altogether, these signals seem to be modulating cellular proliferation and migration via NF-κB, PI3K/Akt/mTOR and MAPK signaling pathways. Further investigation of altered proteins in these pathways may provide more insights on relevant targets, possibly enabling the immunomodulation of tumorigenesis in the aggressive TNBC phenotype. Electronic supplementary material The online version of this article (10.1186/s12864-019-5523-6) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Proteome profiling of triple negative breast cancer cells overexpressing NOD1 and NOD2 receptors unveils molecular signatures of malignant cell proliferation

et al. 2019

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“…They exert the functions of tumor suppressor or facilitator in the progression of human cancers. For example, SPRY4-IT1 can sponge miR-101-3p to expedite cell proliferation and invasion of bladder cancer via regulating EZH2 [9]. NEAT1 exerts the tumor-accelerating functions in esophageal squamous cell carcinoma through miR-129/CTBP2 axis [10].…”

Section: Introductionmentioning

confidence: 99%

LncRNA PCGEM1 accelerates non-small cell lung cancer progression via sponging miR-433-3p to upregulate WTAP

Weng¹,

Qiu²,

Gao³

et al. 2020

BMC Pulm Med

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Background: Non-small cell lung cancer (NSCLC) is one of the most common malignant tumors all over the world. In recent years, long non-coding RNAs (lncRNAs) have been proven to participate in the development of different cancers, including NSCLC. PCGEM1 prostate-specific transcript (PCGEM1) is the lncRNA which is associated with the progression of several cancers. Nevertheless, in NSCLC, the specific functions of PCGEM1 are not yet clear. Methods: The real-time quantitative polymerase chain reaction (qPCR) was utilized to test the expression of PCGE M1 in NSCLC cells. Functional experiments, including cell Counting Kit-8 (CCK-8) assay, 5-ethynyl-2'-deoxyuridine (EdU) assay, flow cytometry analysis and transwell assays were utilized to estimate cell proliferation, migration, invasion and apoptosis. Meanwhile, RNA pull down assay and luciferase reporter assay were utilized to evaluate the correlation of miR-433-3p with PCGEM1 or WT1 associated protein (WTAP). Result: PCGEM1 was highly expressed in NSCLC cells, while miR-433-3p was lowly expressed in NSCLC cells. PCGE M1 silencing or miR-433-3p overexpression inhibited cell proliferation, migration and invasion but accelerated cell apoptosis. MiR-433-3p was proven be sponged by PCGEM1. Besides, WTAP was the target of miR-433-3p and it accelerated the progression of NSCLC. In the end, rescue experiments indicated that overexpression of WTAP or knockdown of miR-433-3p reversed the inhibited roles of silencing PCGEM1 on cell behavior. Conclusions: PCGEM1 accelerates NSCLC progression via sponging miR-433-3p to upregulate WTAP.

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“…Despite advances in surgical techniques and chemotherapeutic agents, the prognosis for OC remains poor, with a 5-year survival rate of <30% (2). The poor prognosis of OC is associated with early metastasis and recurrence (3); it is therefore important to explore the underlying molecular mechanisms associated with ovarian carcinogenesis and progression in order to develop more effective treatment strategies and personalized therapies for OC.…”

Section: Introductionmentioning

confidence: 99%

LncRNA TP73‑AS1 predicts poor prognosis and promotes cell proliferation in ovarian cancer via cell cycle and apoptosis regulation

et al. 2018

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TP73‑AS1, a critical cancer‑associated long noncoding RNA (lncRNA), has been identified in esophageal cancer and glioma. However, its biological role in ovarian cancer (OC) remains to be investigated. The aim of the present study was to investigate the role of TP73‑AS1 in human OC cell lines and clinical tumor samples to determine the function of this molecule. Reverse transcription‑quantitative polymerase chain reaction analysis was carried out to detect that TP73‑AS1 was upregulated in OC tissues and cell lines. Kaplan Meier Method was applied to study the association between overall survival of patients with OC and TP73‑AS1 expression. The results suggested that patients with high expression levels of TP73‑AS1 had lower survival compared with patients with low expression level of TP73‑AS1. MTT and colony formation assays were conducted to investigate the effects of TP73‑AS1 expression on OC cell proliferation. Flow cytometry analysis was used to analyze the effects of TP73‑AS1 expression on cell cycle progression and apoptosis. Loss‑of‑function experiments revealed that TP73‑AS1 silencing was able to suppress the growth of OC cells via modulating the cell cycle and apoptosis. The results of the present study suggest that TP73‑AS1 may be an oncogenic lncRNA that promotes the proliferation of OC cells and may therefore be an effective therapeutic target in patients with OC.

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NUCKS nuclear elevated expression indicates progression and prognosis of ovarian cancer

Cited by 14 publications

References 24 publications

Proteome profiling of triple negative breast cancer cells overexpressing NOD1 and NOD2 receptors unveils molecular signatures of malignant cell proliferation

Proteome profiling of triple negative breast cancer cells overexpressing NOD1 and NOD2 receptors unveils molecular signatures of malignant cell proliferation

LncRNA PCGEM1 accelerates non-small cell lung cancer progression via sponging miR-433-3p to upregulate WTAP

LncRNA TP73‑AS1 predicts poor prognosis and promotes cell proliferation in ovarian cancer via cell cycle and apoptosis regulation

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