LINC00355 promoted the progression of lung squamous cell carcinoma through regulating the miR-466/LYAR axis

Sun, Xuefeng; Wang, Guang-Suo; Ding, Pan; Li, Shixuan

doi:10.1590/1414-431x20209317

Cited by 9 publications

(21 citation statements)

References 37 publications

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“…These results were consistent with the previous studies elevated LINC00355 induced malignant phenotypes, including proliferation, migration and invasion of gastric cancer cells [21]. In LSCC, knockdown of LINC00355 suppressed proliferation, migration and invasion ability in vitro and tumor growth in vivo [31]. Yan et al showed that cancer-associated fibroblasts (CAFs) exosome-mediated transfer of LINC00355 modulated bladder cancer cell proliferation and invasion [32].…”

Section: Discussionsupporting

confidence: 90%

“…Similarly, Zhao et al found that gastric cancer patients with low-expression of LINC00355 had more prolonged survival than patients with LINC00355 high-expression [21]. Sun et al reported that overexpressed LINC00355 positively associated with poor overall survival in lung squamous cell carcinoma (LSCC) patients [31]. Taken together, LINC00355 is up-regulated in bladder cancer patients and correlated with poor prognosis.…”

Section: Discussionmentioning

confidence: 94%

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LncRNA LINC00355 promotes EMT and metastasis of bladder cancer cells through the miR-424-5p/HMGA2 axis

Li¹,

Li²,

Liu³

et al. 2021

neo

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Bladder cancer is a common malignant tumor with a high recurrence rate and mortality, while the detailed mechanisms for bladder cancer progression and metastasis are unknown. Recently, long non-coding RNAs (lncRNAs) are reported to be involved in the development of cancers. In this study, we aim to investigate the role of lncRNA LINC00355 in bladder cancer progression and metastasis. The association between LINC00355 and the prognosis of bladder cancer patients was determined by Kaplan-Meier survival analysis. Cell migration and invasion ability were detected using the Transwell migration and invasion assay. The relationships of LINC00355, miR-424-5p, and High Mobility Group AT-Hook 2 (HMGA2) were verified through the luciferase assay and RNA pull-down assay. Xenograft tumor was established to evaluated tumor lung metastasis in vivo.qRT-PCR and western blot were used to detect gene expression. LINC00355 was upregulated in bladder cancer patients, especially in patients with higher TNM stage. Elevated LINC00355 was correlated with the poor prognosis of bladder cancer patients. Besides, overexpressed LINC00355 promoted migration, invasion, and epithelial-mesenchymal transition (EMT) ability of bladder cancer cells. Contrarily, decreased LINC00355 suppressed migration, invasion, and EMT ability of bladder cancer cells and lung metastasis of xenograft tumors. Furthermore, LINC00355 could regulate HMGA2 expression by acting as a sponge for miR-424-5p. Overexpression of HMGA2 induced EMT of bladder cancer cells. Additionally, LINC00355 regulated the migration, invasion, and EMT ability of bladder cancer cells through modulating HMGA2 expression via sponging miR-424-5p. LINC00355 promoted migration, invasion, and EMT ability of bladder cancer through elevating HMGA2 expression via acting as a sponge for miR-424-5p.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 94%

LncRNA LINC00355 promotes EMT and metastasis of bladder cancer cells through the miR-424-5p/HMGA2 axis

Li¹,

Li²,

Liu³

et al. 2021

neo

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“…28 LINC00355/ miR-466/LYAR ceRNA axis facilitates LUSC development. 29 The binding sites for PITPNA-AS1 were found to be shared by miR-223-3p. MiR-223-3p is involved with a variety of malignancies.…”

Section: Discussionmentioning

confidence: 96%

LncRNA PITPNA‐AS1/miR‐223‐3p/PTN axis regulates malignant progression and stemness in lung squamous cell carcinoma

Peng

Qiu

2022

Clinical Laboratory Analysis

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Background: Long noncoding RNAs (lncRNAs) are a kind of molecule that cannot code proteins, and their expression is dysregulated in diversified cancers. LncRNA PITPNA-AS1 has been shown to act as a tumor promoter in a variety of malignancies, but its function and regulatory mechanisms in lung squamous cell carcinoma (LUSC) are yet unknown. Methods:The mRNA and protein expression of genes were examined by RT-qPCR, western blot, and IHC assay. The cell proliferation, migration, invasion, and stemness were detected through CCK-8, colony formation, Transwell and spheroid formation assays. The CD44 + and CD166 + -positive cells were detected through flow cytometry.The binding ability among genes through luciferase reporter and RNA pull-down assays. The tumor growth was detected through in vivo nude mice assay. Results:The lncRNA PITPNA-AS1 had increased expression in LUSC and was linked to a poor prognosis. In LUSC, PITPNA-AS1 also enhanced cell proliferation, migration, invasion, and stemness. This mechanistic investigation showed that PITPNA-AS1 absorbed miR-223-3p and that miR-223-3p targeted PTN. MiR-223-3p inhibition or PTN overexpression might reverse the inhibitory effects of PITPNA-AS1 suppression on LUSC progression, as demonstrated by rescue experiments. In addition, the PITPNA-AS1/miR-223-3p/PTN axis accelerated tumor development in vivo. Conclusions: It is the first time we investigated the potential role and ceRNA regulatory mechanism of PITPNA-AS1 in LUSC. The data disclosed that PITPNA-AS1 upregulated PTN through sponging miR-223-3p to enhance the onset and progression of LUSC. These findings suggested the ceRNA axis may serve as a promising therapeutic biomarker for LUSC patients.

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“…Therefore, by discovering tumor-related lncRNAs and investigating their involvement in the onset and advancement of cancer, researchers may be able to find new therapeutic and diagnostic biomarkers for LUSC. Several lncRNAs are reported to be up-regulated (69)(70)(71)(72)(73)(74)(75)(76), downregulated (77)(78)(79) in LUSC, and have tumorigenic functions in LUSC pathology. Comparable to protein-coding genes, lncRNAs can be classified as oncogenic or tumor-suppressive.…”

Section: Lncrnas In Luscmentioning

confidence: 99%

“…By targeting miR-466, LINC00355 knockdown inhibited cell proliferation, migration, and invasion, promoted apoptosis in vitro and suppressed tumor development in vivo , therefore downregulating LYAR expression. These studies provide new insight into the molecular processes behind LUSC and suggest that LINC00355 may be utilized as a biomarker for LUSC diagnosis and therapy ( 75 ). Altogether, these findings demonstrate that lncRNAs have a tumor-suppressive function in LUSC.…”

Section: Lncrnas In Luscmentioning

confidence: 99%

Clinicopathological implications of lncRNAs, immunotherapy and DNA methylation in lung squamous cell carcinoma: a narrative review

Sasa¹,

Xuan²,

Chen³

et al. 2021

Transl Cancer Res TCR

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Objective: To explore the clinicopathological impact of lncRNAs, immunotherapy, and DNA methylation in lung squamous cell carcinoma (LUSC), emphasizing their exact roles in carcinogenesis and modes of action.Background: LUSC is the second most prevalent form, accounting for around 30% of non-small cell lung cancer (NSCLC). To date, molecular-targeted treatments have significantly improved overall survival in lung adenocarcinoma patients but have had little effect on LUSC therapy. As a result, there is an urgent need to discover new treatments for LUSC that are based on existing genomic methods. Methods:In this review, we summarized and analyzed recent research on the biological activities and processes of lncRNA, immunotherapy, and DNA methylation in the formation of LUSC. The relevant studies were retrieved using a thorough search of Pubmed, Web of Science, Science Direct, Google Scholar, and the university's online library, among other sources.Conclusions: LncRNAs are the primary components of the mammalian transcriptome and are emerging as master regulators of a number of cellular processes, including the cell cycle, differentiation, apoptosis, and growth, and are implicated in the pathogenesis of a variety of cancers, including LUSC. Understanding their role in LUSC in detail may help develop innovative treatment methods and tactics for LUSC. Meanwhile, immunotherapy has transformed the LUSC treatment and is now considered the new standard of care. To get a better knowledge of LUSC biology, it is critical to develop superior modeling systems. Preclinical models, particularly those that resemble human illness by preserving the tumor immune environment, are essential for studying cancer progression and evaluating novel treatment targets. DNA methylation, similarly, is a component of epigenetic alterations that regulate cellular function and contribute to cancer development.By methylating the promoter regions of tumor suppressor genes, abnormal DNA methylation silences their expression. DNA methylation indicators are critical in the early detection of lung cancer, predicting therapy efficacy, and tracking treatment resistance. As such, this review seeks to explore the clinicopathological impact of lncRNAs, immunotherapy, and DNA methylation in LUSC, emphasizing their exact roles in carcinogenesis and modes of action.

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LINC00355 promoted the progression of lung squamous cell carcinoma through regulating the miR-466/LYAR axis

Cited by 9 publications

References 37 publications

LncRNA LINC00355 promotes EMT and metastasis of bladder cancer cells through the miR-424-5p/HMGA2 axis

LncRNA LINC00355 promotes EMT and metastasis of bladder cancer cells through the miR-424-5p/HMGA2 axis

LncRNA PITPNA‐AS1/miR‐223‐3p/PTN axis regulates malignant progression and stemness in lung squamous cell carcinoma

Clinicopathological implications of lncRNAs, immunotherapy and DNA methylation in lung squamous cell carcinoma: a narrative review

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