LMO4 is a prognostic marker involved in cell migration and invasion in non-small-cell lung cancer

Wang, Wenjun; Wu, Si-Pei; Guo, Meihua; He, Jianxing

doi:10.21037/jtd.2016.12.22

Cited by 15 publications

(14 citation statements)

References 22 publications

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“…In addition, Lmo4 can inhibit differentiation of mammary epithelial cells, and its high expression promotes breast cancer by repressing tumor suppressor BRCA1-mediated transcriptional activation (Visvader et al, 2001; Sum et al, 2002). Lmo4 is also involved in the tumorigenesis of pancreatic cancer (Yu et al, 2008) and non–small cell lung cancer (Wang et al, 2016). Several studies reported that Lmo4 is highly expressed in ILCs and their progenitors (Robinette et al, 2015; Gury-BenAri et al, 2016; Seillet et al, 2016; Harly et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Yeats4 drives ILC lineage commitment via activation of Lmo4 transcription

Liu

Yang

Zhu

et al. 2019

Journal of Experimental Medicine

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Innate lymphoid cells (ILCs) play critical roles in defending infections and maintaining mucosal homeostasis. All ILCs arise from common lymphoid progenitors (CLPs) in bone marrow. However, how CLPs stratify and differentiate into ILC lineages remains elusive. Here, we showed that Yeats4 is highly expressed in ILCs and their progenitors. Yeats4 conditional KO in the hematopoietic system causes decreased numbers of ILCs and impairs their effector functions. Moreover, Yeats4 regulates α4β7+ CLP differentiation toward common helper ILC progenitors (CHILPs). Mechanistically, Yeats4 recruits the Dot1l–RNA Pol II complex onto Lmo4 promoter through recognizing H3K27ac modification to initiate Lmo4 transcription in α4β7+ CLPs. Additionally, Lmo4 deficiency also impairs ILC lineage differentiation and their effector functions. Collectively, the Yeats4–Lmo4 axis is required for ILC lineage commitment.

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Section: Discussionmentioning

confidence: 99%

Yeats4 drives ILC lineage commitment via activation of Lmo4 transcription

Liu

Yang

Zhu

et al. 2019

Journal of Experimental Medicine

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“…LMO4 functioned as an oncogene in diverse cancers, and high expression of LMO4 was linked to poor prognosis and low survival. 29 , 30 In mechanism, LMO4 interacted with proteins involved, among else, in tumorigenesis, such as P53. 31 Besides, a previous study demonstrated that LMO4 was targeted by miR-139-5p, and circRNA-BACH2 facilitated PTC deterioration by activating the expression of LMO4 by targeting miR-139-5p.…”

Section: Discussionmentioning

confidence: 99%

<p>Circ_0058124 Aggravates the Progression of Papillary Thyroid Carcinoma by Activating LMO4 Expression via Targeting miR-370-3p</p>

Liu¹,

Yan²,

Tao³

et al. 2020

CMAR

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Background Thyroid cancer is the most common malignant tumor in the endocrine system. Papillary thyroid carcinoma (PTC) accounts for the vast majority of cases in this cancer. Recently, the vital role of circular RNA (circRNA) has been acknowledged in various cancers, and this study aimed to investigate the role of circ_0058124 and related mechanism of its action in PTC. Materials and Methods The expression of circ_0058124, miR-370-3p and LIM domain only ( LMO4 ) was detected by qRT-PCR in tissue samples (PTC tissues or normal tissues, n=20) and cell lines (non-cancer cell line, Nthy-ori 3–1, and PTC cell lines, IHH-4 and TPC-1). For functional analysis, cell proliferation was investigated using CCK-8 assay and colony formation assay. Cell migration and invasion were determined using transwell assay, and cell migration was also assessed by wound healing assay. Cell apoptosis was monitored by flow cytometry assay. For mechanism analysis, the interaction between miR-370-3p and circ_0058124 or LMO4 predicted by the bioinformatics analysis was validated by dual-luciferase reporter assay or RIP assay. The effect of circ_0058124 on tumor growth in vivo was identified by establishing the Xenograft model. Results The expression of circ_0058124 was enhanced in PTC tissues and cells. Circ_0058124 knockdown inhibited viability, colony formation, migration and invasion and promoted apoptosis of PTC cells. Besides, circ_0058124 knockdown also blocked tumor growth in vivo. miR-370-3p was a target of circ_0058124, and circ_0058124 regulated the expression of LMO4 , a target of miR-370-3p, by targeting miR-370-3p. Rescue experiments presented that miR-370-3p inhibition reversed the inhibitory effects of circ_0058124 knockdown on PTC development, and LMO4 overexpression reversed the effect of miR-370-3p restoration on PTC development. Conclusion Circ_0058124 promoted the development of PTC by mediating the miR-370-3p/ LMO4 axis, and circ_0058124, functioned as an oncogene in PTC, might be used as a promising biomarker for PTC diagnosis and treatment.

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“…Experimentally, LMO4 expression is raised in Burkitt lymphoma cells and LMO4 depression impairs the cell ability of migrating and accelerates cell apoptosis 30 . What is more, it is displayed that LMO4 maintains a high expression in nonsmall cell lung cancer cells and tissues, which is involved in disciplining cell migration and invasion 31 …”

Section: Discussionmentioning

confidence: 99%

“…30 What is more, it is displayed that LMO4 maintains a high expression in nonsmall cell lung cancer cells and tissues, which is involved in disciplining cell migration and invasion. 31…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA small nucleolar RNA host gene 15 deteriorates liver cancer via microRNA‐18b‐5p/LIM‐only 4 axis

et al. 2020

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Extensive studies have explored the involvements of long noncoding RNAs (lncRNAs) in liver cancer. Limitedly, the concrete function of lncRNA small nucleolar RNA host gene 15 (SNHG15) is still elusive. Therefore, the work was initiated to unearth SNHG15-oriented mechanism in liver cancer. Liver cancer tissues were resected. The connection between SNHG15 expression with prognosis and clinicopathological traits of liver cancer patients was evaluated. Liver cancer cells SMMC-7721 were transfected with restored microRNA (miR)-18b-5p or depleted SNHG15 to discover their effects on the proliferation, migration, invasion, cycle arrest, and apoptosis of SMMC-7721 cells. The transfected SMMC-7721 cells were injected into nude mice for further investigation. SNHG15, miR-18b-5p, and LIM-only 4 (LMO4) expressions in tissues and cells were tested. The regulatory connections among SNHG15, miR-18b-5p, and LMO4 were detected. SNHG15 and LMO4 were overexpressed while miR-18b-5p was downregulated in liver cancer tissues and cells. Up-regulated SNHG15 was connected with inferior prognosis and aggressive behaviors of liver cancer patients. SNHG15 knockdown or miR-18b-5p restoration depressed SMMC-7721 cell growth in vivo and in vitro. SNHG15 bound to miR-18b-5p and miR-18b-5p targeted LMO4. The work has illuminated that silencing SNHG15 represses liver cancer progression by modulating miR-18b-5p and LMO4, indicating the therapeutic potency of SNHG15/miR-18b-5p/LMO4 axis in liver cancer.

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LMO4 is a prognostic marker involved in cell migration and invasion in non-small-cell lung cancer

Cited by 15 publications

References 22 publications

Yeats4 drives ILC lineage commitment via activation of Lmo4 transcription

Yeats4 drives ILC lineage commitment via activation of Lmo4 transcription

<p>Circ_0058124 Aggravates the Progression of Papillary Thyroid Carcinoma by Activating LMO4 Expression via Targeting miR-370-3p</p>

Long noncoding RNA small nucleolar RNA host gene 15 deteriorates liver cancer via microRNA‐18b‐5p/LIM‐only 4 axis

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