Silencing of LIMD1 promotes proliferation and reverses cell adhesion‑mediated drug resistance in non‑Hodgkin's lymphoma

Tang, Jie; Zhu, Lin; Huang, Yuejiao; Shi, Bing; Zhang, Shuqing; Gu, Lingli; Zhao, Jie; Deng, Minghao; Zhu, Jiahao; Wang, Yuchan; Wang, Chun

doi:10.3892/ol.2019.9921

Cited by 2 publications

(1 citation statement)

References 32 publications

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“…Results from these different portals show that LIMD1 transcript is significantly downregulated in NSCLC (LUAD and LUSC), uterine corpus endometrial carcinoma (UCEC), and uterine carcinosarcoma (UCS), and upregulated in lymphoid neoplasm diffuse large B-cell lymphoma (DLBC), breast cancer (BRCA), glioblastoma multiforme (GBM), acute myeloid leukemia (LAML), and brain lower-grade glioma (LGG) (Figures 2A-C; Figure 5C; Supplementary Figures 1, 2). In agreement with these results, LIMD1 deregulation was previously found in lung cancer, non-Hodgkin lymphomas, gastric and colorectal carcinomas, and breast cancer (8,(33)(34)(35). The portal Oncomine comprises different datasets with lung cancer clinical or cell line samples, and only those within our statistical power and appropriate controls were selected for analysis (Figure 2).…”

Section: Limd1 Is Downregulated In Nsclcsupporting

confidence: 83%

Algorithm-Based Meta-Analysis Reveals the Mechanistic Interaction of the Tumor Suppressor LIMD1 With Non-Small-Cell Lung Carcinoma

et al. 2021

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Non-small-cell lung carcinoma (NSCLC) is the major type of lung cancer, which is among the leading causes of cancer-related deaths worldwide. LIMD1 was previously identified as a tumor suppressor in lung cancer, but their detailed interaction in this setting remains unclear. In this study, we have carried out multiple genome-wide bioinformatic analyses for a comprehensive understanding of LIMD1 in NSCLC, using various online algorithm platforms that have been built for mega databases derived from both clinical and cell line samples. Our results indicate that LIMD1 expression level is significantly downregulated at both mRNA and protein levels in both lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC), with a considerable contribution from its promoter methylation rather than its gene mutations. The Limd1 gene undergoes mutation only at a low rate in NSCLC (0.712%). We have further identified LIMD1-associated molecular signatures in NSCLC, including its natural antisense long non-coding RNA LIMD1-AS1 and a pool of membrane trafficking regulators. We have also identified a subgroup of tumor-infiltrating lymphocytes, especially neutrophils, whose tumor infiltration levels significantly correlate with LIMD1 level in both LUAD and LUSC. However, a significant correlation of LIMD1 with a subset of immune regulatory molecules, such as IL6R and TAP1, was only found in LUAD. Regarding the clinical outcomes, LIMD1 expression level only significantly correlates with the survival of LUAD (p<0.01) but not with that of LUSC (p>0.1) patients. These findings indicate that LIMD1 plays a survival role in LUAD patients at least by acting as an immune regulatory protein. To further understand the mechanisms underlying the tumor-suppressing function of LIMD1 in NSCLC, we show that LIMD1 downregulation remarkably correlates with the deregulation of multiple pathways that play decisive roles in the oncogenesis of NSCLC, especially those mediated by EGFR, KRAS, PIK3CA, Keap1, and p63, in both LUAD and LUSC, and those mediated by p53 and CDKN2A only in LUAD. This study has disclosed that LIMD1 can serve as a survival prognostic marker for LUAD patients and provides mechanistic insights into the interaction of LIMD1 with NSCLC, which provide valuable information for clinical applications.

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Section: Limd1 Is Downregulated In Nsclcsupporting

confidence: 83%

Algorithm-Based Meta-Analysis Reveals the Mechanistic Interaction of the Tumor Suppressor LIMD1 With Non-Small-Cell Lung Carcinoma

et al. 2021

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Novel hub genes associated with pulmonary artery remodeling in pulmonary hypertension

Tan

You

et al. 2022

Front. Cardiovasc. Med.

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Pulmonary hypertension (PH) is a life-threatening disease with complex pathogenesis. According to etiology, PH is divided into five major groups in clinical classification. However, pulmonary artery (PA) remodeling is their common feature, in addition to bone morphogenetic protein receptor type 2; it is elusive whether there are other novel common genes and similar underlying mechanisms. To identify novel common hub genes involved in PA remodeling at different PH groups, we analyzed mRNA-Seq data located in the general gene expression profile GSE130391 utilizing bioinformatics technology. This database contains PA samples from different PH groups of hospitalized patients with chronic thromboembolic pulmonary hypertension (CTEPH), idiopathic pulmonary artery hypertension (IPAH), and PA samples from organ donors without known pulmonary vascular diseases as control. We screened 22 hub genes that affect PA remodeling, most of which have not been reported in PH. We verified the top 10 common hub genes in hypoxia with Sugen-induced PAH rat models by qRT-PCR. The three upregulated candidate genes are WASF1, ARHGEF1 and RB1 and the seven downregulated candidate genes are IL1R1, RHOB, DAPK1, TNFAIP6, PKN1, PLOD2, and MYOF. WASF1, ARHGEF1, and RB1 were upregulated significantly in hypoxia with Sugen-induced PAH, while IL1R1, DAPK1, and TNFA1P6 were upregulated significantly in hypoxia with Sugen-induced PAH. The DEGs detected by mRNA-Seq in hospitalized patients with PH are different from those in animal models. This study will provide some novel target genes to further study PH mechanisms and treatment.

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Silencing of LIMD1 promotes proliferation and reverses cell adhesion‑mediated drug resistance in non‑Hodgkin's lymphoma

Cited by 2 publications

References 32 publications

Algorithm-Based Meta-Analysis Reveals the Mechanistic Interaction of the Tumor Suppressor LIMD1 With Non-Small-Cell Lung Carcinoma

Algorithm-Based Meta-Analysis Reveals the Mechanistic Interaction of the Tumor Suppressor LIMD1 With Non-Small-Cell Lung Carcinoma

Novel hub genes associated with pulmonary artery remodeling in pulmonary hypertension

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