The Indicative Value of Serum Tumor Markers for Metastasis and Stage of Non-Small Cell Lung Cancer.

Objective: This study aimed to explore the roles of serum tumor markers for metastasis and stage of non-small cell lung cancer (NSCLC). Methods: This study recruited 3272 NSCLC patients admitted to the Tianjin Union Medical Center and the Tianjin Medical University Cancer Institute and Hospital. The predictive abilities of some serum tumor markers (carcinoembryonic antigen (CEA), squamous cell carcinoma antigen (SCC-Ag), cytokeratin-19 fragment (CYFRA 21-1), neuron-specific enolase (NSE), pro-gastrin-releasing peptide (ProGRP), total prostate-specific antigen (TPSA) and carbohydrate antigen 199 (CA199)) for NSCLC metastasis (intrapulmonary, lymphatic and distant metastasis) and clinical stage were analyzed. Results: Tumor markers exhibited different numerical and proportional distributions in NSCLC patients. Elevated CEA, CYFRA 21-1 and CA199 levels were indicative of tumor metastasis and stage. Increased CEA and CA199 provided an accurate prediction of intrapulmonary and distant metastasis with the area under the receiver operator characteristic curve (AUC) of 0.69 both (p < 0.001); Increased CEA, CYFRA 21-1 and CA199 provided an accurate prediction of lymphatic metastasis with the AUC of 0.62 (p < 0.001). Conclusion: Combined detection of serum tumor markers can indicate tumor metastasis and stage in NSCLC patients.

Integrated Bioinformatics Analysis Identifies a New Stemness Index-Related Survival Model for Prognostic Prediction in Lung Adenocarcinoma.

BACKGROUND: Lung adenocarcinoma (LUAD) is one of the most lethal malignancies and is currently lacking in effective biomarkers to assist in diagnosis and therapy. The aim of this study is to investigate hub genes and develop a risk signature for predicting prognosis of LUAD patients. METHODS: RNA-sequencing data and relevant clinical data were downloaded from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) database. Weighted gene co-expression network analysis (WGCNA) was performed to identify hub genes associated with mRNA expression-based stemness indices (mRNAsi) in TCGA. We utilized LASSO Cox regression to assemble our predictive model. To validate our predictive model, me applied it to an external cohort. RESULTS: mRNAsi index was significantly associated with the tissue type of LUAD, and high mRNAsi scores may have a protective influence on survival outcomes seen in LUAD patients. WGCNA indicated that the turquoise module was significantly correlated with the mRNAsi. We identified a 9-gene signature (CENPW, MCM2, STIL, RACGAP1, ASPM, KIF14, ANLN, CDCA8, and PLK1) from the turquoise module that could effectively identify a high-risk subset of these patients. Using the Kaplan-Meier survival curve, as well as the time-dependent receiver operating characteristic (tdROC) analysis, we determined that this gene signature had a strong predictive ability (AUC = 0.716). By combining the 9-gene signature with clinicopathological features, we were able to design a predictive nomogram. Finally, we additionally validated the 9-gene signature using two external cohorts from GEO and the model proved to be of high value. CONCLUSION: Our study shows that the 9-gene mRNAsi-related signature can predict the prognosis of LUAD patient and contribute to decisions in the treatment and prevention of LUAD patients.

Extracellular vesicles promotes liver metastasis of lung cancer by ALAHM increasing hepatocellular secretion of HGF.

Tumor-derived extracellular vesicles (EVs) are involved in tumor metastasis. Highly enriched lncRNA-ALAHM was identified from serum EVs of lung adenocarcinoma (LUAD) patients with liver metastasis by high-throughput sequencing. A mouse model of in situ lung cancer was used to determine the effect of ALAHM in LUAD cell EVs on liver metastasis. The effects of ALAHM on hepatocyte paracrine HGF as well as proliferation, invasion, and migration of LUAD cells were observed in vitro. As results, ALAHM expression in LUAD cell EVs was significantly increased. LUAD-cell-derived EVs overexpressing ALAHM significantly promoted lung cancer liver metastasis in model mice. ALAHM of LUAD cell EVs also promotes hepatocyte parasecretion of HGF by binding with AUF1 and increases the proliferation, invasion, and migration of LUAD cells. Thus, LUAD-cell-derived EVs containing ALAHM causes increasing HGF and promoting liver metastasis of LUAD cells.

High TSPAN8 expression in epithelial cancer cell-derived small extracellular vesicles promote confined diffusion and pronounced uptake.

Small extracellular vesicles (sEVs) play a key role in intercellular communication. Cargo molecules carried by sEVs may affect the phenotype and function of recipient cells. Epithelial cancer cell-derived sEVs, particularly those enriched in CD151 or tetraspanin8 (TSPAN8) and associated integrins, promote tumour progression. The mechanism of binding and modulation of sEVs to recipient cells remains elusive. Here, we used genetically engineered breast cancer cells to derive TSPAN8-enriched sEVs and evaluated the impact of TSPAN8 on target cell membrane's diffusion and transport properties. The single-particle tracking technique showed that TSPAN8 significantly promoted sEV binding via confined diffusion. Functional assays indicated that the transgenic TSPAN8-sEV cargo increased cancer cell motility and epithelial-mesenchymal transition (EMT). In vivo, transgenic TSPAN8-sEV promoted uptake of sEVs in the liver, lung, and spleen. We concluded that TSPAN8 encourages the sEV-target cell interaction via forced confined diffusion and significantly increases cell motility. Therefore, TSPAN8-sEV may serve as an important direct or indirect therapeutic target.

Tumor-associated exosomes promote lung cancer metastasis through multiple mechanisms.

As an important medium of intercellular communication, exosomes play an important role in information transmission between tumor cells and their microenvironment. Tumor metastasis is a serious influencing factor for poor treatment effect and shortened survival. Lung cancer is a major malignant tumor that seriously threatens human health. The study of the underlying mechanisms of exosomes in tumor genesis and development may provide new ideas for early and effective diagnosis and treatment of lung cancer metastasis. Many studies have shown that tumor-derived exosomes promote lung cancer development through a number of processes. By promoting epithelial-mesenchymal transition of tumor cells, they induce angiogenesis, establishment of the pretransfer microenvironment, and immune escape. This understanding enables researchers to better understand the mechanism of lung cancer metastasis and explore new treatments for clinical application. In this article, we systematically review current research progress of tumor-derived exosomes in metastasis of lung cancer. Although positive progress has been made toward understanding the mechanism of exosomes in lung cancer metastasis, systematic basic research and clinical translational research remains lacking and are needed to translate our scientific understanding toward applications in the clinical diagnosis and treatment of lung cancer metastasis in the near future.

DeepCSO: A Deep-Learning Network Approach to Predicting Cysteine S-Sulphenylation Sites.

Cysteine S-sulphenylation (CSO), as a novel post-translational modification (PTM), has emerged as a potential mechanism to regulate protein functions and affect signal networks. Because of its functional significance, several prediction approaches have been developed. Nevertheless, they are based on a limited dataset from Homo sapiens and there is a lack of prediction tools for the CSO sites of other species. Recently, this modification has been investigated at the proteomics scale for a few species and the number of identified CSO sites has significantly increased. Thus, it is essential to explore the characteristics of this modification across different species and construct prediction models with better performances based on the enlarged dataset. In this study, we constructed several classifiers and found that the long short-term memory model with the word-embedding encoding approach, dubbed LSTM WE , performs favorably to the traditional machine-learning models and other deep-learning models across different species, in terms of cross-validation and independent test. The area under the receiver operating characteristic (ROC) curve for LSTM WE ranged from 0.82 to 0.85 for different organisms, which was superior to the reported CSO predictors. Moreover, we developed the general model based on the integrated data from different species and it showed great universality and effectiveness. We provided the on-line prediction service called DeepCSO that included both species-specific and general models, which is accessible through http://www.bioinfogo.org/DeepCSO.

lnc-REG3G-3-1/miR-215-3p Promotes Brain Metastasis of Lung Adenocarcinoma by Regulating Leptin and SLC2A5.

This study aims to explore the role and mechanism of specific lncRNA in brain metastasis (BM) from lung adenocarcinoma (LADC), providing an effective biomarker for early diagnosis and targeted therapy of BM from LADC. Based on the gene expression profiles of lncRNA and mRNA in LADC and BM tissues detected by Gene Chip, lnc-REG3G-3-1 was selected, and the related genes, including miR-215-3p, leptin, and SLC2A5, were identified by data analysis. Human LADC cell lines A549 and H1299 were cultured. Dual-luciferase and endogenous validation experiments were used to confirm the regulation between these genes. Real-time quantitative reverse transcription-polymerase chain reaction and Western blotting were used to detect gene expression. The tumor metastasis-related gene function of lnc-REG3G-3-1 and miR-215-3p in H1299 cells was verified by Transwell invasion, migration assays, and scratch testing. Nude mice xenograft tumors constructed with decreased lnc-REG3G-3-1 confirmed the influences on gene expression in vivo. lnc-REG3G-3-1 was highly expressed in BM tissues that originated from LADC compared with that in primary cancer tissues. lnc-REG3G-3-1 reduced miR-215-3p expression, thereby regulating the target genes leptin and SLC2A5 and the signaling pathways, taking part in the lnc-REG3G-3-1/miR-215-3p axis in the process of BM from LADC. lnc-REG3G-3-1, leptin, and SLC2A5 through regulating signaling pathways may be jointly involved in the regulation of the biological process of BM in patients with LADC.

The endometrium histopathology and cell ultrastructure in bitches with pyometra induced using progesterone and Escherichia coli.

BACKGROUND: We investigated uterine histopathological and ultrastructural changes in female dogs with pyometra induced by Escherichia coli (E. coli) inoculation using progesterone and/or estradiol. METHODS: Dogs were ovariectomized and classified into six groups: Groups 1-6 corresponding to estradiol treatment followed by progesterone supplementation, progesterone supplementation only, estradiol supplementation only, simultaneous treatment using estradiol and progesterone, similar to Group 1 but with a double dose, and control group, respectively. RESULTS: Pyometra was successfully induced in Groups 1, 2, 4, and 5, but not in Group 3. An uneven endometrial surface was observed, along with a purulent discharge, bleeding, inflammatory lesions, cystic endometrial hyperplasia (CEH) or cystic endometrial atrophy. Endometrial thickness percentage, uterine wall thickness, and the percentage of endometrial cyst area increased. Endometrial epithelial mushroom-like hyperplasia and the honeycomb-like structure exposed under the epithelium after flaky exfoliation were found, and the glandular epithelial villi became longer or shorter. Mitochondria expansion and increased lysosome were observed. Endoplasmic reticulum dilation and swelling and many inflammatory cells, especially plasma cell infiltration in the stroma, were found. CONCLUSIONS: Endometrial histopathology and ultrastructural changes in affected dogs were accompanied by induction of pyometra, and they were affected by different hormonal patterns and E. coli.

Importance of Effective Regulation for the Chinese Genetic Testing Industry.

The genetic testing industry is progressing rapidly. In particular, the demand of patients with tumors for diagnosis, treatment, and testing drives genetic testing to develop further. Simultaneously, the potential risks of genetic testing cause severe challenges to regulatory departments. In China, a targeted, clear, and unified management model remains absent.

Application of CRISPR/Cas9 gene editing technique in the study of cancer treatment.

In recent years, gene editing, especially that using clustered regularly interspaced short palindromic repeat (CRISPR)/Cas9, has made great progress in the field of gene function. Rapid development of gene editing techniques has contributed to their significance in the field of medicine. Because the CRISPR/Cas9 gene editing tool is not only powerful but also has features such as strong specificity and high efficiency, it can accurately and rapidly screen the whole genome, facilitating the administration of gene therapy for specific diseases. In the field of tumor research, CRISPR/Cas9 can be used to edit genomes to explore the mechanisms of tumor occurrence, development, and metastasis. In these years, this system has been increasingly applied in tumor treatment research. CRISPR/Cas9 can be used to treat tumors by repairing mutations or knocking out specific genes. To date, numerous preliminary studies have been conducted on tumor treatment in related fields. CRISPR/Cas9 holds great promise for gene-level tumor treatment. Personalized and targeted therapy based on CRISPR/Cas9 will possibly shape the development of tumor therapy in the future. In this study, we review the findings of CRISPR/Cas9 for tumor treatment research to provide references for related future studies on the pathogenesis and clinical treatment of tumors.

Applications of CRISPR/Cas9 Technology in the Treatment of Lung Cancer.

Since its emergence, the application of CRISPR-associated nuclease 9 (Cas9) technology in cancer research has accelerated studies to investigate many aspects of treatment approaches for lung cancer, including the identification of target genes, construction of animal tumor models, and identification of drug resistance-related genes. Moreover, CRISPR/Cas9 can be used in gene therapy for lung cancer, specifically involving molecular targeted drugs and inhibitors. This article reviews the current landscape of CRISPR/Cas9 applications for lung cancer treatment as a basis for further studies. Given its promising performance, in-depth and systematic research on the application of CRISPR/Cas9 in lung cancer treatment will be necessary in future studies for its successful implementation in clinical practice.

Rare ectopic metastasis from clear cell renal cell carcinoma to the chest wall after 10 years: A case report.

RATIONALE: Clear cell renal cell carcinoma (CCRCC) is an aggressive tumor associated with a high risk of metastasis and very low survival rate. In addition, it can cause extensive blood metastasis to the lungs, bones, and other organs. Chest wall metastatic tumors from primary CCRCC are rare. PATIENT CONCERNS: In this report, we present a case of metastatic chest wall tumor that originated from a CCRCC. DIAGNOSES: An 86-year-old man was diagnosed with chest wall tumor using chest computed tomography. After collecting tissues from the chest wall tumor via needle biopsy, the pathological examination was combined with positive immunoreaction of CD10, epithelial membrane antigen, and vimentin, and the patient was diagnosed with metastatic CCRCC in the chest wall deposits. INTERVENTIONS: The patient received radiotherapy at 2.0 Gy per time for 25 times. OUTCOMES: Following 2 months of treatment, the chest wall tumor had shrunk by about one-third of its size. LESSONS: Our patient developed a metastatic chest wall tumor that originated from a CCRCC for which right nephrectomy had been performed 10 years previously. Although as per the literature, chest wall metastasis from CCRCC is very rare, it is important to consider tumor metastasis after several years of treatment for precise diagnosis and proper treatment.

Oxidative stress-elicited autophagosome accumulation contributes to human neuroblastoma SH-SY5Y cell death induced by PBDE-47.

Polybrominated diphenyl ethers, a ubiquitous persistent organic pollutant used as brominated flame retardants, is known to damage nervous system, however the underlying mechanism is still elusive. In this study, we used human neuroblastoma SH-SY5Y cells to explore the effects of PBDE-47 on autophagy and investigate the role of autophagy in PBDE-47-induced cell death. Results showed PBDE-47 could increase autophagic level (performation of cell ultrastructure with double membrane formation, MDC-positive cells raised, autophagy-related proteins LC3-II, Beclin1 and P62 increased) after cells exposed to PBDE-47. Then cells were exposed to PBDE-47 (1, 5, 10µmol/L) respectively for 1, 3, 6, 9, 12, 18, 24h, and the results showed that PBDE-47 increased the levels of LC3-II, Beclin1 and P62 in 5, 10µmol/L (9, 12, 18, 24h) PBDE-47 exposed groups. Furthermore, ROS scavenger N-Acetyl-l-cysteine (NAC), autophagic inhibitor 3-methyladenine (3-MA) and 5µmol/L PBDE-47 treated for 9h and 24h were chosen for the follow-up research. Moreover, 3-MA significantly improved cell viability when cells exposed to 5 and 10µmol/L PBDE-47, indicating that PBDE-47-induced autophagic cell death. Importantly, NAC could decrease PBDE-47-induced LC3-II, Beclin1 and P62 expression. We concluded that autophagosome accumulation mediated by oxidative stress may contribute to SH-SY5Y cell death induced by PBDE-47.

Potential lung carcinogenicity induced by chronic exposure to PM2.5 in the rat.

Exposure to fine particulate matter (PM2.5) may increase lung cancer risk, but the underlying mechanisms are poorly understood. This study explored the potential carcinogenicity in rat lung induced by chronic exposure to PM2.5. Adult male rats (200-220 g) were treated with PM2.5 (10 mg/kg body weight) by tracheal perfusion once per week for 1 year; the rats were killed, and expression of tumor markers (carcinoembryonic antigen (CEA), neuron-specific enolase (NSE), squamous cell carcinoma antigen (SCCA)), cancer-related genes, and pathological changes were detected. Chronic treatment with PM2.5 significantly increased SCCA and NSE expression in rat lung tissue and serum. Damaged lung tissue structure was observed by hematoxylin and eosin staining. Although no evidence of tumors was detected, the Wnt/ß-catenin signaling, epithelial-mesenchymal transition, vascular endothelial growth factor, and epidermal growth factor receptor pathways were all activated or overexpressed and likely involved in the potential carcinogenicity in the rat model. Additionally, abnormal expression of the proto-oncogenes c-Myc and K-Ras and tumor suppressor p53 can be seen in lung tissue induced by PM2.5 exposure. Chronic exposure to PM2.5 has the potential to be carcinogenic in rat lung.

WIF-1 gene inhibition and Wnt signal transduction pathway activation in NSCLC tumorigenesis.

The aim of the present study is to explore the differential expression of key molecules associated with Wnt signaling in both clinical non-small cell lung cancer (NSCLC) tissue and adjacent normal lung tissue, and to discuss the tumorigenic role of the activation of Wnt signaling pathways in NSCLC. A total of 52 NSCLC patients were employed in the present study. Lung cancer tissue samples and paracarcinoma tissue samples were obtained from these patients, who had undergone surgical resection of their primary cancer. The cases were diagnosed by hematoxylin and eosin staining. Using reverse transcription-quantitative polymerase chain reaction and immunohistochemical straining, the messenger RNA (mRNA) and protein expression levels of Wnt inhibitory factor-1 (WIF-1) and important molecules associated with Wnt signaling pathways were detected. Compared with normal tissues, a marked decreased in the mRNA and protein expression levels of WIF-1, and an increase in ß-catenin and cyclin D1 expression, were observed in tumor tissues. This suggests that the activation of the Wnt/ß-catenin signaling pathway may be closely associated with lymph nodal metastasis and lower pathological classification. However, no obvious difference could be observed in adenomatous polyposis coli (APC) expression levels between lung cancer tissues and adjacent tissues to the carcinoma. The activation of the Wnt/ß-catenin signaling pathway in NSCLC could be initiated by WIF-1 gene inhibition without APC expression changes, and this may be different to the mechanism in other tumors.

Hypermethylation of IFN-γ in oral cancer tissues.

OBJECTIVES: The study aimed to evaluate the methylation pattern of the interferon-gamma (IFN-γ) gene in oral cancer tissues compared with normal and benign oral disease tissues. MATERIALS AND METHODS: The oral tissues were gained from the patients of 85 cases of oral squamous cell carcinoma (OSCC), 47 cases of oral dysplastic lesions, and 53 normal biopsies. IFN -γ methylation in oral tissues was verified through methylation-specific polymerase chain reaction (PCR) and DNA sequencing analyses, and the expression levels of IFN-γ messenger RNA (mRNA) and protein were detected using real-time reverse transcription (RT)-PCR and enzyme-linked immunosorbent assays, respectively. IFN-γ was localized in macrophages from oral tissues and detected via immunostaining. RESULTS: IFN-γ mRNA and protein expression levels were evidently decreased in oral cancer tissues, whereas the IFN-γ methylation rate was significantly higher in malignant tumors than in benign and normal tissues (normal, 22.6%; benign, 38.3%; and cancer, 55.3%; P < 0.05). Furthermore, the expression of IFN-γ mRNA was significantly downregulated in oral tumors with methylation compared with tumors without methylation, as determined by real-time RT-PCR (4.76-fold difference; P < 0.05). Likewise, mRNA expression was downregulated by 6.79-fold in oral epithelial dysplasia tissues with methylation compared with those without methylation (P < 0.01). Co-immunostaining to detect MAC2 and IFN-γ demonstrated that macrophages comprised the main source of IFN-γ in oral tissues. IFN-γ methylation demonstrated a significant association with the clinical stage, histopathology grade, and primary tumor. CONCLUSIONS: Aberrant IFN-γ promoter methylation may be involved in the process of tumorigenesis of oral cancer. CLINICAL RELEVANCE: IFN-γ hypermethylation during the process of oral carcinogenesis could be useful for the clinical diagnosis and treatment for OSCC.

Inhibition of KLF5-Myo9b-RhoA Pathway-Mediated Podosome Formation in Macrophages Ameliorates Abdominal Aortic Aneurysm.

RATIONALE: Abdominal aortic aneurysms (AAAs) are characterized by pathological remodeling of the aortic wall. Although both increased Krüppel-like factor 5 (KLF5) expression and macrophage infiltration have been implicated in vascular remodeling, the role of KLF5 in macrophage infiltration and AAA formation remains unclear. OBJECTIVE: To determine the role of KLF5 in AAA formation and macrophage infiltration into AAAs. METHODS AND RESULTS: KLF5 expression was significantly increased in human AAA tissues and in 2 mouse models of experimental AAA. Moreover, in myeloid-specific Klf5 knockout mice (myeKlf5-/- mice), macrophage infiltration, medial smooth muscle cell loss, elastin degradation, and AAA formation were markedly decreased. In cell migration and time-lapse imaging analyses, the migration of murine myeKlf5-/- macrophages was impaired, and in luciferase reporter assays, KLF5 activated Myo9b (myosin IXB) transcription by direct binding to the Myo9b promoter. In subsequent coimmunostaining studies, Myo9b was colocalized with filamentous actin, cortactin, vinculin, and Tks5 in the podosomes of phorbol 12,13-dibutyrate-treated macrophages, indicating that Myo9b participates in podosome formation. Gain- and loss-of-function experiments showed that KLF5 promoted podosome formation in macrophages by upregulating Myo9b expression. Furthermore, RhoA-GTP levels increased after KLF5 knockdown in macrophages, suggesting that KLF5 lies upstream of RhoA signaling. Finally, Myo9b expression was increased in human AAA tissues, located in macrophages, and positively correlated with AAA size. CONCLUSIONS: These data are the first to indicate that KLF5-dependent regulation of Myo9b/RhoA is required for podosome formation and macrophage migration during AAA formation, warranting consideration of the KLF5-Myo9b-RhoA pathway as a therapeutic target for AAA treatment.

Long non-coding RNAs: potential new biomarkers for predicting tumor invasion and metastasis.

Long non-coding RNAs (lncRNAs) play important roles in malignant neoplasia. Indeed, many hallmarks of cancer define that the malignant phenotype of tumor cells are controlled by lncRNAs. Despite a growing number of studies highlighting their importance in cancer, there has been no systematic review of metastasis-associated lncRNAs in various cancer types. Accordingly, we focus on the key metastasis-related lncRNAs and outline their expression status in cancer tissues by reviewing the previous stuides, in order to summarize the nowadays research achivements for lncRNAs related to cancer metastasis. Medline, EMBASE, as well as PubMed databases were applied to study lncRNAs which were tightly associated with tumor invasion and metastasis. Up to now, a substantial number of lncRNAs have been found to have important biological functions. In this review, according to their various features in cancer, lncRNAs were roughly divided into three categories: promoting tumor invasion and metastasis, negative regulation of tumor metastasis and with dual regulatory roles. The present studies may establish the foundation for both further research on the mechanisms of cancer progression and future lncRNA-based clinical applications.

Screening for the Key lncRNA Targets Associated With Metastasis of Renal Clear Cell Carcinoma.

A large number of long noncoding RNAs (lncRNAs) have been found to be implicated in varieties of tumors. However, the contributions of lncRNAs to tumorigenesis in renal clear cell carcinoma (RCCC) remain largely unknown.We performed a genome-wide analysis of lncRNA expression in RCCC and matched nontumor (NT) tissues to identify new targets for further study of renal carcinoma.The genome-wide analysis of lncRNA expression in 3 RCCC and matched NT tissues were conducted using 4 × 180K Agilent lncRNA Chips and 6 lncRNAs were selected and validated by qRT-PCR in 90 RCCC patients. The differentially expressed lncRNAs and mRNAs were recognized through P value and fold-change (FC) filtering. Potential targets associated with RCCC were identified by gene ontology and pathway analyses. Construction of the co-expression network was accomplished using Cytoscape.A total of 3862 lncRNAs and 2935 mRNAs were deregulated in RCCC tissues, compared with paired NT tissues. PCR results showed the expressions of these 6 lncRNAs were consistent with the chips. Moreover, the co-expression network analysis portended 641 nodes and 571 connections between 109 lncRNAs and 532 coding genes. Lastly, NONHSAT123350 could be involved in the pathogenesis of RCCC and its expression level was closely related to disease-free survival (DFS) and overall survival (OS) in patients without distant metastasis.Our results indicated that these abnormal lncRNAs could respond to renal carcinoma progression and NONHSAT123350 may act as a potential target for future treatment of RCCC.