LncARSR promotes glioma tumor growth by mediating glycolysis through the STAT3/HK2 axis.

BACKGROUND: Glioma represents the predominant malignant brain tumor. This investigation endeavors to elucidate the impact and prospective mechanisms of glycolysis-related lncARSR on glioma. METHODS: LncARSR level was assessed in normal glial cells and glioma cells. Cell proliferation, migration, and invasion measurements were conducted through CCK-8, wound healing, and transwell assay. Flow cytometry was utilized to measure cell apoptosis and cell cycle. Biochemical assay kits and immunoblotting were employed to measure the content of glycolysis-related indicators and protein expression, respectively. We analyzed the impact of both lncARSR knockdown and overexpression of the Signal Transducer and Activator of Transcription 3 (STAT3) on Hexokinase 2 (HK2) using dual luciferase reporter assays and Chromatin Immunoprecipitation (ChIP) experiments. Further assessment of the impact of lncARSR on glioma progression was conducted through animal experiments. RESULTS: LncARSR was expressed at elevated levels in glioma cells compared to normal glial cells. Overexpressing lncARSR enhanced proliferation, migration, invasion, and G2/M phase arrest in glioma cells and also increased glucose, lactate, ATP production, as well as the expression of HK2, PFK1, PKM2, GLUT1, and LDHA. STAT3 binding to the HK2 gene promoter was weakened following the knockdown of lncARSR. Upregulation of STAT3 reversed the suppressed functions of knocking down lncARSR on cell proliferation, migration, invasion, G2/M phase arrest, and glycolysis and counteracted its promotional effect on cell apoptosis. In vivo, knocking down lncARSR inhibits glioma growth and ki67 and PCNA expression. CONCLUSION: LncARSR promotes the development of glioma by enhancing glycolysis through the STAT3-HK2 axis.

The lncARSR/PTEN/Akt/nuclear factor-kappa B feedback regulatory loop contributes to doxorubicin resistance in hepatocellular carcinoma.

Chemoresistance is a major obstacle to hepatocellular carcinoma (HCC) chemotherapy. Our previous study found that long noncoding RNA lncARSR (lncRNA Activated in RCC with Sunitinib Resistance) activated Akt signaling via repressing phosphatase and tensin homolog (PTEN) during doxorubicin resistance in HCC. The purpose of this study is to further explore lncARSR-mediated mechanisms and roles during doxorubicin resistance in HCC. The expression of lncARSR was detected by real-time quantitative polymerase chain reaction (qPCR). Nuclear factor-kappa B (NF-κB) activity was detected by NF-κB luciferase reporter assays, western blot, and NF-κB transcription factor assays. The effects of NF-κB on lncARSR were detected by chromatin immunoprecipitation assay, promoter luciferase reporter assay, and real-time qPCR. The effects of lncARSR/Akt/NF-κB on doxorubicin resistance were detected by Cell Counting Kit-8 assay, capsase-3 activity assay, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay. lncARSR activated NF-κB signaling through activation of Akt. NF-κB transactivated lncARSR through directly binding lncARSR promoter and increasing lncARSR promoter activity. Akt transactivated lncARSR via activating NF-κB signaling. Thus, lncARSR, Akt, and NF-κB formed a positive feedback regulatory loop in HCC. Through this feedback loop, lncARSR auto-regulated its transcription. Drug sensitivity assays showed that the lncARSR/Akt/NF-κB feedback regulatory loop promoted doxorubicin resistance in HCC. These findings identified the lncARSR/Akt/NF-κB feedback regulatory loop in HCC, which represent potential therapeutic targets for improving doxorubicin sensitivity in HCC.

Long noncoding RNA lncARSR promotes nonalcoholic fatty liver disease and hepatocellular carcinoma by promoting YAP1 and activating the IRS2/AKT pathway.

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is the main cause for hepatocellular carcinoma (HCC). This study was intended to identify the function of long non-coding RNA (lncRNA) lncARSR in NAFLD and its role in human HCC cells (HepG2) proliferation and invasion. METHODS: LncARSR expression was detected both in high fatty acid-treated HepG2 cells and NAFLD mouse model. After gain- and loss-of-function approaches in high fatty acid-treated HepG2 cells and NAFLD mice, lipid accumulation in livers from NAFLD mice and high fatty acid-treated cells was determined by H&E staining, Oil Red-O staining or Nile Red staining respectively. Expression of YAP1, adipogenesis- (Fasn, Scd1 and GPA) and IRS2/AKT pathway-related genes was measured. Cell proliferation was monitored by MTT and soft-agar colony formation assays, cell cycle was analyzed by flow cytometry, and cell invasion was examined by transwell assay. The tumor weight and volume were then measured through in vivo xenograft tumor model after silencing lncARSR. RESULTS: LncARSR was highly expressed in high fatty diet (HFD)-fed mice and high fatty acid-treated HepG2 cells. LncARSR was observed to bind to YAP1, which inhibited phosphorylation nuclear translocation. LncARSR activated the IRS2/AKT pathway by reducing YAP1 phosphorylation, and further increased lipid accumulation, cell proliferation, invasion and cell cycle. Silencing lncARSR in HFD-fed mice alleviated NAFLD by regulating YAP1/IRS2/AKT axis. CONCLUSION: Silencing lncARSR suppressed the IRS2/AKT pathway, consequently reducing HCC cell proliferation and invasion and inhibiting lipid accumulation in NAFLD mice by downregulating YAP1, which suggests a clinical application in treating NAFLD.

Long noncoding RNA lncARSR promotes hepatic lipogenesis via Akt/SREBP-1c pathway and contributes to the pathogenesis of nonalcoholic steatohepatitis.

Non-alcoholic fatty liver disease and steatohepatitis (NAFLD and NASH) account for the majority of liver disease in industrialized countries. However, the pathogenesis still unclear. Long non-coding RNAs (lncRNAs) has been reported to be involved in various pathophysiological processes. Here, we reported a novel role of lncARSR in hepatic lipogenesis in NAFLD. The expression of lncARSR was induced both in NAFLD patients and mouse model, as well as in hepatocytes treated with fatty acid. Moreover, overexpression of lncARSR enhanced while knockdown of lncARSR ameliorated hepatic lipid accumulation in vivo and in vitro. Furthermore, the expression of genes related to fatty acid synthesis and oxidation increased with lncARSR overexpression in vivo. Mechanistically, we identified that lncARSR regulated hepatic lipogenesis via upregulating SREBP-1c, the key regulatory molecule involved in lipogenesis. Knockdown of SREBP-1c by shRNA blocked the effect of lncARSR on lipogenesis. Furthermore, we demonstrated that lncARSR regulated SREBP-1c expression by PI3K/Akt pathway. In conclusion, our data indicated that lncARSR potentially contributes to the hepatic steatosis in NAFLD, which may be a new therapeutic target against NAFLD.

Long Noncoding RNA lncARSR Promotes Doxorubicin Resistance in Hepatocellular Carcinoma via Modulating PTEN-PI3K/Akt Pathway.

Hepatocellular carcinoma (HCC) is generally resistant to chemotherapy due to intrinsic or acquired drug resistances. Many molecules and signaling pathways are involved in chemo-resistance of HCC cells. However, the contribution of long noncoding RNA (lncRNA) to chemo-resistance of HCC cells is still largely unknown. In this study, we revealed the critical roles of long noncoding RNA lncARSR in chemo-resistance of HCC cells. lncARSR is upregulated in HCC, associated with large tumor size and advanced BCLC stage, and indicts poor prognosis. Functional assays showed that overexpression of lncARSR enhances doxorubicin resistance of HCC cells in vitro and in vivo. And while knockdown of lncARSR increases sensitivity of HCC cells to doxorubicin in vitro and in vivo. Mechanistically, we found that lncARSR physically associates with PTEN mRNA, promotes PTEN mRNA degradation, decreases PTEN expression, and activates PI3K/Akt pathway. PTEN is downregulated in HCC, and the expression of PTEN is negatively correlated with lncARSR in HCC tissues. Furthermore, the effects of lncARSR overexpression on doxorubicin resistance could be reversed by PI3K/Akt pathway inhibitor, and lncARSR knockdown-induced doxorubicin sensitivity could be reversed by PTEN depletion. Taken together, our results showed that upregulated lncARSR promotes doxorubicin resistance in HCC via modulating PTEN-PI3K/Akt pathway, and implied that lncARSR may serve as a promising prognostic biomarker and therapeutic target for HCC chemo-resistance. J. Cell. Biochem. 118: 4498-4507, 2017. © 2017 Wiley Periodicals, Inc.

METTL3-induced lncARSR aggravates neuroblastoma tumorigenic properties through stabilizing PHOX2B.

Neuroblastoma (NB), the most common extracranial solid tumor in pediatric patients, manifests with considerable variability across multiple primary sites. Despite this, the extent of genetic heterogeneity within these tumor foci and the identification of consistent oncogenic drivers remains largely unexplored. Of particular interest, genetic mutations in PHOX2B have been linked to familial cases of NB, yet the underlying molecular mechanisms are not fully delineated. In our research, we focus on unraveling the role of a novel functional long non-coding RNA (lncRNA) associated with PHOX2B in the context of NB. Using NB cell models with overexpressed PHOX2B, combined with lncRNA microarray analysis, we discovered that lncARSR is significantly upregulated in response to PHOX2B overexpression. Subsequent biological assays demonstrated that lncARSR promotes both the proliferation and metastasis of NB cells. Further molecular investigations revealed that lncARSR plays a crucial role in stabilizing PHOX2B expression within NB cells. Moreover, we identified that the expression of lncARSR is regulated by methylation through methyltransferase-like 3 (METTL3), which itself is positively correlated with PHOX2B expression. Rescue experiments underscored the functional importance of METTL3, lncARSR, and PHOX2B in NB cells. In summary, our findings provide new insights into the molecular functions of PHOX2B in the progression of neuroblastoma and propose a novel therapeutic target for this aggressive malignancy.

Roles of LncRNA ARSR in tumor proliferation, drug resistance, and lipid and cholesterol metabolism.

Cancer is one of the most serious diseases that threaten human life and health. Among all kinds of diseases, the mortality rate of malignant tumors is the second highest, second only to cardio-cerebrovascular diseases. Cancer treatment typically involves imaging, surgery, and pathological analysis. When patients are identified as carcinoma by the above means, there are often problems of distant metastasis, delayed treatment, and drug tolerance, indicating that patients have some poor prognosis and overall survival. Hence, the development of novel molecular biomarkers is of great clinical importance. In recent years, as an important mediator of material and information exchange between cells in the tumor microenvironment, lncRNA have attracted widespread attention for their roles in tumor development. In this review, we comprehensively summarize the up-to-date knowledge of lncARSR on diverse cancer types which mainly focuses on tumor proliferation, drug tolerance, and lipid and cholesterol metabolism, highlighting the potential of lncARSR as a diagnostic and prognostic biomarker and even a therapeutic target. In our final analysis, we provide a synthesized overview of the directions for future inquiry into lncARSR, and we are eager to witness the advancement of research that will elucidate the multifaceted nature of this lncRNA.

Renal cell carcinoma-derived exosomes deliver lncARSR to induce macrophage polarization and promote tumor progression via STAT3 pathway.

Tumor-derived exosomes play a pivotal role in regulating tumor progression by mediating crosstalk between tumor cells and immune cells such as macrophages within the tumor microenvironment. Macrophages can adopt two distinct polarization statuses and switch between M1 or M2 activation phenotypes in response to the different external stimuli. However, the role of tumor derived exosomes in the macrophage phenotypic switch and tumor development have not been elucidated in renal cell carcinoma (RCC). Here we found that high macrophage infiltration was associated with worse prognosis in RCC patients, therefore we propose our hypothesis that RCC derived exosomes might directly influence macrophage polarization and thus promote tumor progression. Both cell-based in vitro models and orthotopic transplantation in vivo tumor models were constructed and ELISA, flow cytometry, and macrophage functional studies were performed to investigate whether and how RCC-derived exosomes regulate macrophage polarization and tumor growth. The results found that these exosomes promote macrophage polarization, cytokine release, phagocytosis, angiogenesis, and tumor development. Further study revealed high amount of a recently discovered lncRNA called lncARSR in RCC-derived exosomes. Overexpression of lncARSR induced phenotypic and functional changes of macrophages in vitro and promoted tumor growth in vivo, while knockdown of lncARSR by siRNA disrupted the exosomes-mediated macrophage polarization. LncARSR interacts directly with miR-34/miR- 449 to increase STAT3 expression and mediate macrophage polarization in RCC cells. Together, RCC-derived exosomes facilitate the development of tumor through inducing macrophage polarization via transferring lncARSR, suggesting that RCC-derived exosomes, lncARSR and STAT3 are the potential therapeutic targets for treatment of RCC.

[Balectin-3 affects the stability of vulnerable coronary atherosclerosis plaques by targeted modulation of lncARSR].

OBJECTIVE: To investigate the mechanism by which galectin-3 (Gal-3) affects the stability of vulnerable coronary atherosclerosis plaques through long non-coding RNA ARSR (lncARSR). METHOD: Male BALB/c mice were randomly divided into normal diet group, high-fat diet group, high-fat diet+lncARSR inhibitor group (n=20). The high-fat diet contained 15% fat and 0.25% cholesterol, and lncARSR inhibitor was injected intravenously at 50 nmol/L every other day. After 12 weeks of high-fat diet feeding and treatment, the mice were euthanized for analyzing coronary atherosclerosis and plaque damage using Sudan IV and oil red O staining. The protein expressions of Gal-3 and ARSR in the coronary artery of the mice were analyzed with Western blotting, and the expressions of PI3K and Akt were detected with immunohistochemistry. The coronary artery tissues were harvested from normal mice for cell culture, and the isolated cells were transfected with a Gal-3 mimic or a Gal-3 inhibitor. At 24 h after the transfection, dual luciferase reporter gene assay was performed to determine the target relationship between Gal-3 and lncARSR; the mRNA expressions of tumor necrosis factor (TNF-α), interleukin-ß (IL-ß) and IL-6 in the transfected cells were detected with RT-qPCR. RESULTS: The positively stained areas by Sudan IV and red oil O and the protein expression of lncARSR were the lowest in normal diet group and the highest in high-fat diet group (P < 0.05). The protein expression of PI3K and Akt and the mRNA expression of TNF-α, IL-ß and IL-6 in high-fat diet group were higher than those in normal diet group. The protein expression of PI3K and Akt and the mRNA expression of TNF-α, IL-ß and IL-6 in high-fat diet+ lncARSR inhibitor group were significantly lower than those in high-fat diet group (P < 0.05). In the cell experiment, the activity of WT-lncARSR was significantly higher in Gal-3 mimic transfection group than in the control group and Gal-3 inhibition group (P=0.026), and was the lower in Gal-3 inhibition group than in the control group (P=0.017). CONCLUSION: Gal-3 and lncARSR are overexpressed in coronary atherosclerosis. Through a mechanism for targeted inhibition of lncARSR, Gal-3 regulates the PI3K/ Akt signaling pathway to suppress inflammation and thus regulate the stability of vulnerable coronary atherosclerosis plaques.

LncARSR promotes non-small-cell lung cancer progression via regulating PTEN/Akt.

LncRNAs have been suggested to be key modulators in many biological and pathological processes. LncARSR, a recently identified lncRNA, plays crucial roles in the progression of several cancers. However, the role of lncARSR in NSCLC is uninvestigated. In the present study, it was demonstrated that lncARSR expression was higher in NSCLC tissues than in noncancerous tissues. The expression of lncARSR was higher in four NSCLC cell lines than in a normal lung bronchial epithelial line. Further investigation demonstrated that increased lncARSR expression promoted NSCLC cell migration and growth and induced epithelial-mesenchymal transition in A549 cells. Moreover, ectopic expression of lncARSR suppressed PTEN expression and induced Akt phosphorylation in A549 cells. The expression level of PTEN was higher in NSCLC samples than in adjacent non-tumor specimens. PTEN expression was negatively correlated with lncARSR in NSCLC specimens. Furthermore, we demonstrated that overexpression of lncARSR induced NSCLC cell growth and migration via regulating the PTEN/Akt signaling pathway. These results suggest that lncARSR acts as an oncogene in NSCLC development and could serve as a new potential therapeutic target.

LncARSR sponges miR-129-5p to promote proliferation and metastasis of bladder cancer cells through increasing SOX4 expression.

Emerging evidences have indicated that long non-coding RNAs (lncRNAs) are potential biomarkers, playing important roles in the development of cancer. LncRNA Activated in RCC with Sunitinib Resistance (lncARSR) is a novel lncRNA that functions as a potential biomarker and is involved in the progression of cancers. However, the clinical significance and molecular mechanism of lncARSR in bladder cancer (Bca) remains unknow. In this study, we discovered that lncARSR was significantly up-regulated in bladder cancer. In addition, increased expression of lncARSR was positively correlated with higher histological grade and larger tumor size. Further experiments demonstrated that suppression of lncARSR attenuated the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) process of Bca cells. Mechanistically, lncARSR was mainly located in the cytoplasm and acted as a miRNA sponge to positively modulate the expression of Sex-determining region Y-related high-mobility-group box transcription factor 4 (SOX4) via sponging miR-129-5p and subsequently promoted the proliferation and metastasis of Bca cells, thus playing an oncogenic role in Bca pathogenesis. In conclusion, our study indicated that lncARSR plays a critical regulatory role in Bca cells and lncARSR may serve as a potential diagnostic biomarker and therapeutic target for bladder cancer.

Genetic variants in a long noncoding RNA related to Sunitinib Resistance predict risk and survival of patients with renal cell carcinoma.

OBJECTIVE: LncARSR (lncRNA Activated in RCC with Sunitinib Resistance, ENST00000424980) is a newly identified lncRNA to promote the sunitinib resistance of renal cell carcinoma (RCC), which may contribute to tumorigenesis and progression. This study aimed to explore the association of lncARSR tagSNPs with the risk and prognosis of RCC. METHODS: In this study, a 2-stage case-control study was performed to evaluate the association between 2 tagging SNPs (rs1417080 and rs7859384) and RCC susceptibility. Odds ratios (ORs) and 95% confidence intervals (CIs) were obtained by unconditional logistic regression analyses. Different survival time was estimated by the Kaplan-Meier method and compared by the Log-rank test. Hazard ratios (HRs) and their 95% CIs were calculated to determine predictive factors by Cox proportion hazards model. RESULTS: When combing discovery and validation sets together, rs7859384 was determined to be significantly associated with the decreased RCC risk with all P < 0.05 in 4 models (co-dominant model, additive model, dominant model and recessive model). stratified analyses showed prominent risk effect of SNP rs7859384 GA/GG genotypes was found in clinical subgroups of stage I and stage II (P = 0.009, OR = 0.77, 95% CI = 0.64-0.94) and individuals with clear cell RCC (P = 0.014, OR = 0.79, 95% CI = 0.65-0.95). A protective effect of SNP rs7859384 GA/GG genotypes was observed among individuals with BMI > 24 (P = 0.025, OR = 0.74, 95% CI = 0.56-0.96), without hypertension (P = 0.037, OR = 0.79, 95% CI = 0.63-0.99), without family history of cancer (P = 0.048, OR = 0.83, 95% CI = 0.68-1.00). Survival analyses revealed individuals with GA/GG genotypes had higher survival rate compared with the corresponding AA wild genotypes in the dominant model (log-rank P = 0.005, adjusted HR = 0.34, 95% CI = 0.16-0.73). CONCLUSION: This study suggests that rs7859384 of lncARSR was associated with RCC susceptibility and may act as a prognostic biomarker for patients with RCC.

lncARSR promotes liver cancer stem cells expansion via STAT3 pathway.

Liver cancer stem cells (CSCs) have important functions in tumorigenesis, progression, recurrence and drug resistance of hepatocellular carcinoma (HCC). lncARSR has been reported to play an important role in the maintenance and self-renewal of renal cancer stem cells, but its role in liver cancer stem cells (CSCs) remains obscure. Herein, we observed high expression of lncARSR in chemoresistant hepatocellular carcinomas (HCCs). A remarkable increase of lncARSR expression in EpCAM or CD133-positive liver CSCs as well as in CSC-enriched hepatoma spheres. Interference lncARSR suppressed liver CSC expansion by inhibiting the dedifferentiation of hepatoma cells and decreasing the self-renewal ability of liver CSCs. Mechanistically, we found STAT3 as the downstream of lncARSR in HCC cells. The special STAT3 inhibitor S3I-201 abolished the discrepancy in liver CSC proportion and the self-renewal capacity between lncARSR knockdown hepatoma cells and control cells, which further confirmed that STAT3 was required in lncARSR promoted liver CSCs expansion. More importantly, interference lncARSR HCC cells were more sensitive to sorafenib or cisplatin treatment. This maybe means that patients with low lncARSR levels benefited from cisplatin or sorafenib treatment, but patients with high lncARSR expression did not. Conclusion: lncARSR was upregulated in liver CSCs and could promote HCC cells dedifferentiation and liver CSCs expansion by targeting STAT3 signaling.

Long noncoding RNA lncARSR promotes epithelial ovarian cancer cell proliferation and invasion by association with HuR and miR-200 family.

Epithelial ovarian cancer (EOC) is the fifth leading cause of female cancer-related deaths worldwide. Long non-coding RNAs (lncRNAs) are emerging as crucial regulators in various biological processes through diverse mechanisms. Recently, lncRNA Activated in RCC with Sunitinib Resistance (lncARSR) has been reported to be upregulated and involved in sunitinib resistance of renal cell carcinoma cells. However, the functional roles in EOC have not yet been explored. In the current study, we detected the expression levels of lncARSR in 76 paired EOC tissues and adjacent normal tissues, and observed that lncARSR expression was significantly increased in EOC tissues and correlated with FIGO stage, histological grade, lymph nodes metastasis and worse survival. Loss- and gain-of-function assays demonstrated that lncARSR promoted EOC cell proliferation and invasion. Further investigations showed that lncARSR interacted with HuR, upregulated ß-catenin expression and then activated Wnt/ß-catenin signaling pathway to regulate cell proliferation. Moreover, lncARSR increased ZEB1 and ZEB2 expression by competitively binding the miR-200 family to induce EMT and invasion. Our findings suggest that the lncARSR may provide a novel therapeutic strategy for EOC treatment.

Long noncoding RNA lncARSR promotes hepatic cholesterol biosynthesis via modulating Akt/SREBP-2/HMGCR pathway.

AIMS: Disruption of cholesterol homeostasis has been identified as a major factor in the pathogenesis of atherosclerosis, myocardial infarction, and strokes. Long noncoding RNAs (lncRNAs) have emerged as critical players in cellular cholesterol metabolism, but their functions are still largely unknown. MATERIALS AND METHODS: C57BL6/j mice were fed with high cholesterol diet (containing 4% cholesterol) or chow diet. Adenoviruses-lncARSR and lncARSR shRNA were used to overexpress or knockdown lncARSR expression. KEY FINDINGS: The expression of lncARSR were increased both in patients with hypercholesterolemia and mice with high cholesterol diet feeding. Overexpression of lncARSR in mice resulted in elevated lipid levels in both serum and liver fragments. However, knockdown of lncARSR in mice fed with high cholesterol diet showed decreased lipid levels in serum and liver fragments compared with control mice. Furthermore, we found that the expression of HMG-CoA reductase (HMGCR), the rate-limiting enzyme of cholesterol synthesis was increased with lncARSR overexpression, which was accompanied with the increase of hepatic de novo cholesterol synthesis rate. Mechanistically, we found that lncARSR increased the expression of mature SREBP-2, which is a primary transcription factor of HMGCR. And lncARSR activated the PI3K/Akt pathway. When PI3K/Akt pathway was blocked by LY294002, the inhibitor of PI3K, the effect of lncARSR on SREBP-2 and HMGCR disappeared. SIGNIFICANCE: Our data indicated upregulated lncARSR promotes hepatic cholesterol biosynthesis via modulating Akt/SREBP-2/HMGCR pathway, and implied that lncARSR may serve as a therapeutic target for cholesterol disorder.

Research progress on the correlation between lncARSR and malignant tumors / 中国肿瘤生物治疗杂志

@#[摘 要] 长链非编码RNA（lncRNA）ARSR（lncARSR）作为lncRNA家族中的成员之一，近年来受到医学界的广泛关注。随着lncARSR相关基础及临床研究的逐渐深入，发现其不仅在多种生物学过程包括脂代谢中起重要的调控作用，同时在恶性肿瘤的发生、发展及治疗过程的耐药性中均发挥类似癌基因的功能。研究发现，lncARSR在多种类型肿瘤患者的血清、组织及细胞中呈高表达，而且通过调控靶基因进而促进肿瘤细胞增殖、侵袭及转移，抑制肿瘤细胞凋亡，增强肿瘤耐药性，与肿瘤的分期及预后密切相关，为肿瘤的早期诊断及生物治疗提供了新的思路。综述中论述了lncARSR在结直肠癌、卵巢癌、非小细胞肺癌、膀胱癌、肾细胞癌、肝细胞癌和骨肉瘤等恶性肿瘤中的作用及其机制的相关性研究进展。