lncRNA MNX1‑AS1 promotes prostate cancer progression through regulating miR‑2113/MDM2 axis

Dong, Liang; Tian, Chuanjie; Zhang, Xiaowen

doi:10.3892/mmr.2022.12747

Cited by 11 publications

(6 citation statements)

References 41 publications

(44 reference statements)

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“…Until now, the miRNAs implicated in sepsis-induced ALI are largely unknown. miR-2113 has been reported to mediate cell proliferation and apoptosis [ 10 , 25 ]. In this research, we supplied compelling evidence supporting the function of miR-2113 in sepsis-induced ALI.…”

Section: Discussionmentioning

confidence: 99%

MiR-2113 overexpression attenuates sepsis-induced acute pulmonary dysfunction, inflammation and fibrosis by inhibition of HMGB1

Li,

Xu,

Kang

et al. 2024

Heliyon

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Section: Discussionmentioning

confidence: 99%

MiR-2113 overexpression attenuates sepsis-induced acute pulmonary dysfunction, inflammation and fibrosis by inhibition of HMGB1

Li,

Xu,

Kang

et al. 2024

Heliyon

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“…The sodium pentobarbital was mixed with sterile saline to make a 3% solution and injected intraperitoneally at a dose of 50 mg/kg (1-1.25 mg per mouse). 25 The mice were sacrificed by cervical dislocation and mortality was confirmed by cessation of heartbeat. The excised tumors were weighed at 4 weeks.…”

Section: Methodsmentioning

confidence: 99%

TRIM11 Posttranscriptionally Modulated by miR-5193 Facilitates Tumor Growth and Metastasis of Prostate Cancer

Pan

2023

Technol Cancer Res Treat

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Objective Tripartite motif-containing protein 11 (TRIM11), an E3 ubiquitin ligase, possesses a pro-tumor property. Still, the detailed functions of TRIM11 remain not well characterized in prostate cancer. Methods PC-3 and DU145 prostate cancer cells were transfected with small interfering RNAs (siRNAs) or lentiviruses for TRIM11 deficiency or overexpression, and microRNA-5193 (miR-5193) mimics were utilized for overexpressing miR-5193. Proliferation, apoptosis, migration, and invasion were examined through CCK-8, colony formation, flow cytometry, wound healing, and transwell assays. MAP kinase-extracellular signal-regulated kinase (MEK1/2) and extracellular signal-regulated kinase (ERK)1/2 activities were detected via immunoblotting. Murine xenograft models were established. Interactions of TRIM11 with miR-5193 were demonstrated via dual luciferase reporter. Results TRIM11 deficiency or miR-5193 overexpression exerted antiprostate cancer effects through suppression of proliferation, migration, and invasion as well as enhancement of apoptosis in PC-3 and DU145 cells. The mechanisms by which TRIM11 deficiency or miR-5193 overexpression involved the inactivation of MEK1/2 and ERK1/2. miR-5193 downregulated TRIM11 expressions in prostate cancer cells, and their interactions were confirmed. Further, up-regulated miR-5193 weakened the effects of TRIM11 overexpression on enhancing proliferation, migration, invasion, and activity of MEK1/2 and ERK1/2 as well as alleviating apoptosis of prostate cancer cells. In murine xenograft models, TRIM11 upregulation facilitated tumor growth, which was alleviated by miR-5193 overexpression. Conclusion These findings described the oncogenic role of TRIM11 in prostate cancer biology, which was post-transcriptionally modulated by miR-5193.

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“…Researchers have found that prostate cancer is closely related to the expression of lncRNAs. For example, the expression of MAGI2-AS3 and MEG3 in lncRNAs inhibits the development of prostate cancer [60,61], and MNX1-AS1 indirectly promotes the development of prostate cancer through expression [62]. We used it as the second disease in the case study, and the experimental outcomes are presented in Table 9.…”

Section: Case Studymentioning

confidence: 99%

Node-adaptive graph Transformer with structural encoding for accurate and robust lncRNA-disease association prediction

Li,

Bai,

Liang

et al. 2023

Preprint

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Background Long noncoding RNAs (lncRNAs) are integral to a plethora of critical cellular biological processes, including the regulation of gene expression, cell differentiation, and the development of tumors and cancers. Predicting the relationships between lncRNAs and diseases can contribute to a better understanding of the pathogenic mechanisms of disease and provide strong support for the development of advanced treatment methods.Results Therefore, we present an innovative node-adaptive Transformer model for predicting unknown associations between lncRNAs and diseases (GNATLDA). First, we utilize the node-adaptive feature smoothing (NAFS) method to learn the local feature information of nodes and encode the structural information of the fusion similarity network of diseases and lncRNAs using Structural Deep Network Embedding (SDNE). Next, the Transformer module, which contains a multi-headed attention layer, is used to learn global feature information about the nodes of the heterogeneous network, which is used to capture potential association information between the network nodes. Finally, we employ a Transformer module with two multi-headed attention layers for learning global-level embedding fusion. Network structure coding is added as the structural inductive bias of the network to compensate for the missing message-passing mechanism in Transformer. Our model accounts for both local-level and global-level node information and exploits the global horizon of the Transformer model, which fuses the structural inductive bias of the network to comprehensively investigate unidentified associations between nodes, significantly increasing the predictive effectiveness of potential interactions between diseases and lncRNAs. We conducted case studies on four diseases; 55 out of 60 interactions between diseases and lncRNAs were confirmed by the literature.Conclusions Our proposed GNATLDA model can serve as a highly efficient computational method for predicting biological information associations.

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lncRNA MNX1‑AS1 promotes prostate cancer progression through regulating miR‑2113/MDM2 axis

Cited by 11 publications

References 41 publications

MiR-2113 overexpression attenuates sepsis-induced acute pulmonary dysfunction, inflammation and fibrosis by inhibition of HMGB1

MiR-2113 overexpression attenuates sepsis-induced acute pulmonary dysfunction, inflammation and fibrosis by inhibition of HMGB1

TRIM11 Posttranscriptionally Modulated by miR-5193 Facilitates Tumor Growth and Metastasis of Prostate Cancer

Node-adaptive graph Transformer with structural encoding for accurate and robust lncRNA-disease association prediction

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