LncRNA LINC00511 promotes COL1A1-mediated proliferation and metastasis by sponging miR-126-5p/miR-218-5p in lung adenocarcinoma

Wang, Yudong; Mei, Xingke; Song, Weikang; Wang, Chen; Qiu, Xueshan

doi:10.1186/s12890-022-02070-3

Cited by 16 publications

(16 citation statements)

References 40 publications

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“…The studies reported here also revealed that STIP1 and miR-218-5p are inversely correlated, and the transfection of OSCC cell lines with miR-218-5p mimics downregulated STIP1 which was followed by inhibition of proliferation, motility and invasiveness, similarly as seen with STIP1 silencing. Recently, miR-218-5p was reported to be downregulated in several cancers, including gastric, colorectal, ovarian, prostate, cervical and lung adenocarcinoma ( 41 – 46 ) and have different protein targets affecting cancer progression. Downregulation of miR-218-5p promoted OSCC invasion via activating CD44-ROCK signaling ( 47 ).…”

Section: Discussionmentioning

confidence: 99%

Stress induced phosphoprotein 1 overexpression controls proliferation, migration and invasion and is associated with poor survival in oral squamous cell carcinoma

et al. 2023

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ObjectiveAlthough there have been remarkable achievements in the molecular landscape of oral squamous cell carcinoma (OSCC) in recent years, bringing advances in the understanding of its pathogenesis, development and progression, little has been applied in the prognosis and choosing the optimal treatment. In this study, we explored the influence of the stress induced phosphoprotein 1 (STIP1), which is frequently reported to be highly expressed in many cancers, in OSCCs.MethodsSTIP1 expression was assessed in the TCGA database and in two independent cohorts by immunohistochemistry. Knockdown strategy was applied in OSCC cell lines to determine the impact of STIP1 on viability, proliferation, migration and invasion. The zebrafish model was applied for studying tumor formation and metastasis in vivo. The association of STIP1 and miR-218-5p was explored by bioinformatics and mimics transfection.ResultsSTIP1 was highly expressed in OSCCs and significantly associated with shortened survival and higher risk of recurrence. STIP1 down-regulation decreased proliferation, migration and invasion of tumor cells, and reduced the number of metastases in the Zebrafish model. STIP1 and miR-218-5p were inversely expressed, and the transfection of miR-218-5p mimics into OSCC cells decreased STIP1 levels as well as proliferation, migration and invasion.ConclusionOur findings show that STIP1 overexpression, which is inversely associated with miR-218-5p levels, contributes to OSCC aggressiveness by controlling proliferation, migration and invasion and is a determinant of poor prognosis.

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Section: Discussionmentioning

confidence: 99%

Stress induced phosphoprotein 1 overexpression controls proliferation, migration and invasion and is associated with poor survival in oral squamous cell carcinoma

et al. 2023

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“…In addition, Linc00511 is known to activate the PI3K/AKT signaling pathway by upregulating COL1A1. 17 The latter was identified as a prognostic gene in LUAD, and was significantly upregulated at both the mRNA and protein levels. 18 The increase in COL1A1 expression is positively correlated with that of NOTCH3.…”

Section: Discussionmentioning

confidence: 99%

“…Linc00511 can enhance the COL1A1‐mediated proliferation of LUAD cells by acting as a sponge for miRNA. In addition, Linc00511 is known to activate the PI3K/AKT signaling pathway by upregulating COL1A1 17 . The latter was identified as a prognostic gene in LUAD, and was significantly upregulated at both the mRNA and protein levels 18 .…”

Section: Discussionmentioning

confidence: 99%

Single‐cell transcriptome analysis reveals intratumoral heterogeneity in lung adenocarcinoma

Xu,

Jiang,

Qin

et al. 2023

Environmental Toxicology

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IntroductionLung adenocarcinoma (LUAD) is a major health concern worldwide. Single‐cell RNA‐sequencing (scRNA‐seq) provides a valuable platform for exploring the intratumoral heterogeneity in LUAD and holds great potential for facilitating the development and application of personalized therapeutic approaches.MethodsThe TCGA‐LUAD (n = 503), GSE68465 (n = 442), GSE72094 (n = 398), and GSE26939 (n = 115) datasets were retrieved for prognostic assessment. Subgroup analysis was performed for the epithelial cells, endothelial cells, immune cells, and fibroblasts, and the transcription factors and tumor‐related pathways enriched in each subgroup were analyzed using PROGENy and DoRothEA package. The InferCNV software was used to calculate the copy number variations (CNVs) in tumor cell subgroups with normal epithelial cells as the reference. The association between the annotated cell types and survival was analyzed using the Scissor software.ResultsWe identified eight major cell types in LUAD, namely epithelial cells, NK cells, T and B cells, endothelial cells, mast cells, myeloid cells, and fibroblasts, of which the epithelial cells and B cells showed a marked increase in the tumor samples. In addition, we also detected an intense signal transduction network from the cancer‐associated fibroblasts (CAFs) to malignant cells, mainly involving the DCN/MET, COLA1/DDR1, COL1A1/SDC1, and COL1A2/SDC1 pathways. The tumor differentiation trajectory consisted of state 1 and state 2, which were enriched in HIF1A, and state 4. Furthermore, only a few B cells originated from the normal tissue, suggesting significant recruitment and infiltration of B cells in LUAD. Based on differentially upregulated genes in the cells positively and negatively associated with survival, we established a prognostic model that showed satisfactory predictive performance in three different cohorts. States 3 and 2 of epithelial cells included the majority of cells with KRAS mutation, whereas state 2 showed high frequency of EGFR mutations.ConclusionWe analyzed intra‐tumor heterogeneity of LUAD at the single‐cell level and developed a prognostic index that was highly effective across multiple cohorts.

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“…In several types of cancer, most lncRNAs are either up- or downregulated. These lncRNAs favor all stages of tumor development through the promotion of mRNA expression and constancy [ 253 ], by favoring mRNA stability [ 254 ], or by modulating miR [ 254 , 255 , 256 , 257 , 258 , 259 , 260 , 261 , 262 , 263 , 264 , 265 , 266 , 267 , 268 , 269 , 270 , 271 , 272 , 273 , 274 , 275 , 276 , 277 , 278 , 279 , 280 , 281 , 282 , 283 , 284 , 285 , 286 , 287 , 288 , 289 , 290 , 291 , 292 , 293 , 294 , 295 , 296 , 297 , 298 , 299 , 300 ]. The aberrant phenotype is the result of the modulation of typical pathways playing key roles in cell survival [ 255 , 259 , 263 , 265 , 283 ], apoptosis [ <...…”

Section: Analyzing Cernets For Diagnosis and Targeting Them For Thera...mentioning

confidence: 99%

“…Another important pathway in cancer is the phosphoinositide 3-kinase-AKT-mammalian target of the rapamycin (PI3K-AKT-mTOR) pathway, which is frequently hyperactivated in cancer and is essential for tumor cell growth and survival [ 61 ]. Indeed, several lncRNAs such as HOTAIR, HOXD-AS1, LINC00511, H19, and LINC01554, by targeting specific miRs, increase the expression of AKT and mTOR, promoting aberrant phenotypes [ 262 , 264 , 271 , 274 , 278 , 287 , 296 ].…”

Section: Analyzing Cernets For Diagnosis and Targeting Them For Thera...mentioning

confidence: 99%

Using ncRNAs as Tools in Cancer Diagnosis and Treatment—The Way towards Personalized Medicine to Improve Patients’ Health

Piergentili

Basile

Nocella

et al. 2022

IJMS

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Although the first discovery of a non-coding RNA (ncRNA) dates back to 1958, only in recent years has the complexity of the transcriptome started to be elucidated. However, its components are still under investigation and their identification is one of the challenges that scientists are presently facing. In addition, their function is still far from being fully understood. The non-coding portion of the genome is indeed the largest, both quantitatively and qualitatively. A large fraction of these ncRNAs have a regulatory role either in coding mRNAs or in other ncRNAs, creating an intracellular network of crossed interactions (competing endogenous RNA networks, or ceRNET) that fine-tune the gene expression in both health and disease. The alteration of the equilibrium among such interactions can be enough to cause a transition from health to disease, but the opposite is equally true, leading to the possibility of intervening based on these mechanisms to cure human conditions. In this review, we summarize the present knowledge on these mechanisms, illustrating how they can be used for disease treatment, the current challenges and pitfalls, and the roles of environmental and lifestyle-related contributing factors, in addition to the ethical, legal, and social issues arising from their (improper) use.

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LncRNA LINC00511 promotes COL1A1-mediated proliferation and metastasis by sponging miR-126-5p/miR-218-5p in lung adenocarcinoma

Cited by 16 publications

References 40 publications

Stress induced phosphoprotein 1 overexpression controls proliferation, migration and invasion and is associated with poor survival in oral squamous cell carcinoma

Stress induced phosphoprotein 1 overexpression controls proliferation, migration and invasion and is associated with poor survival in oral squamous cell carcinoma

Single‐cell transcriptome analysis reveals intratumoral heterogeneity in lung adenocarcinoma

Using ncRNAs as Tools in Cancer Diagnosis and Treatment—The Way towards Personalized Medicine to Improve Patients’ Health

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