miR-1182-mediated ALDH3A2 inhibition affects lipid metabolism and progression in ccRCC by activating the PI3K-AKT pathway.

In clear cell renal cell carcinoma (ccRCC), dysregulated lipid metabolism plays a pivotal role in tumor initiation and progression. This study delves into the unexplored landscape of Dysregulated Aldehyde Dehydrogenase 3 Family Member A2 (ALDH3A2) in ccRCC. Using a combination of "fatty acid metabolism" dataset analysis and differentially expressed genes (DEGs) derived from Gene Expression Omnibus (GEO) database, potential metabolic regulators in ccRCC were identified. Subsequent investigations utilizing public databases, clinical samples, and in vitro experiments revealed that ALDH3A2 was down-regulated in ccRCC, mediated by miR-1182, highlighting its role as an independent prognostic factor for patient survival. Functionally, ALDH3A2 exhibited tumor-suppressive properties, impacting ccRCC cell phenotypes and influencing epithelial-mesenchymal transition. Mechanistically, silencing ALDH3A2 promoted lipid accumulation in ccRCC cells by activating the PI3K-AKT pathway, thereby promoting tumor progression. These findings shed light on the critical role of the miR-1182/ALDH3A2 axis in ccRCC tumorigenesis, emphasizing the potential for targeting lipid metabolism as a promising anti-cancer strategy.

lncRNA FAM230B is highly expressed in colorectal cancer and suppresses the maturation of miR-1182 to increase cell proliferation.

Long non-coding RNA FAM230B and microRNA (miR-1182) have been characterized as critical players in cancer biology, while their roles in colorectal cancer (CRC) are unclear. We predicted that they could interact with each other and therefore explored the interaction between them in CRC. CRC and paired non-tumor tissue samples were collected from 60 CRC patients, and the expression of FAM230B and miR-1182 (premature and mature) in these samples was analyzed with RT-qPCR. The direct interaction between FAM230B and premature miR-1182 was analyzed with RNA-RNA pull-down assay, and the subcellular location of FAM230B was detected with subcellular fractionation assay. The interaction between FAM230B and miR-1182 was explored with overexpression assay, and their roles in regulating CRC cell proliferation, viability, and colony formation were assessed by BrdU assay, MTT assay, and colony formation assay, respectively. We found that FAM230B and premature miR-1182 were highly upregulated in CRC, while mature miR-1182 was downregulated in CRC. FAM230B was detected in both nucleus and cytoplasm, and it directly interacted with miR-1182. FAM230B overexpression increased the expression levels of premature miR-1182 but decreased the expression levels of mature miR-1182 in CRC cells. FAM230B promoted CRC cell proliferation, increased cell viability, accelerated colony formation, and suppressed the role of miR-1182 in inhibiting CRC cell proliferation. In conclusion, FAM230B is upregulated in CRC and it suppresses the maturation of miR-1182 to promote tumor growth.

Circ_0002476 regulates cell growth, invasion, and mtDNA damage in non-small cell lung cancer by targeting miR-1182/TFAM axis.

BACKGROUND: Many circular RNAs (circRNAs) have been identified as potential targets for cancer therapy. However, the role of circ_0002476 in non-small cell lung cancer (NSCLC) progression has not been explored. METHODS: The expression levels of circ_0002476, microRNA (miR)-1182, and mitochondrial transcription factor A (TFAM) were detected by quantitative real-time polymerase chain reaction. Cell functions were measured by cell counting kit 8 assay, EdU assay, colony formation assay, flow cytometry and transwell assay. Mitochondrial DNA (mtDNA) damage was assessed by measuring mtDNA copy number and transcript levels of ND1 and ATP6. Protein expression was examined by western blot. The interaction between miR-1182 and circ_0002476 or TFAM was detected by dual-luciferase reporter assay and RNA pull-down assay. Animal experiments were performed to explore circ_0002476 role in vivo. Exosomes (Exs) were extracted and identified by transmission electron microscopy and nanoparticle tracking analysis. RESULTS: Circ_0002476 was overexpressed in NSCLC tissues and cells. Circ_0002476 knockdown suppressed NSCLC cell proliferation and invasion, while promoted apoptosis and mtDNA damage. Circ_0002476 could sponge miR-1182, and miR-1182 inhibitor reversed the influence induced by circ_0002476 knockdown. Moreover, TFAM was targeted by miR-1182, and miR-1182 hindered NSCLC cell progression by regulating TFAM. Additionally, circ_0002476 silencing could reduce NSCLC tumor growth by miR-1182/TFAM. Further analyzed showed that Exs were involved in the transport of circ_0002476 between cells. CONCLUSION: Taken together, our findings suggested that circ_0002476 might be a potential molecular target for NSCLC treatment.

Circ_0061395 functions as an oncogenic gene in hepatocellular carcinoma by acting as a miR-1182 sponge.

Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in liver cancer, with a high rate of metastasis and recurrence. Circular RNA_0061395 (circ_0061395) has been shown to be involved in the advance of HCC. However, the interaction between circ_0061395 and microRNA (miRNA) in HCC has not been studied. Quantitative real-time polymerase-chain reaction (qRT-PCR) was used to detect the expression of related genes in liver cancer tissues and cells. The stability of circ_0061395 was verified by RNase R digestion. Through detection of cell malignant behavior and apoptosis, the capping experiment was carried out to verify the regulatory relationship between miR-1182 and circ_0061395 or SPARC/osteonectin, CWCV and Kazal-like domains proteoglycan 1 (SPOCK1). The expression of related proteins was detected by western blot. The interaction of miR-1182 with circ_0061395 or SPOCK1 has been notarized by Dual-luciferase reporter analysis and RNA immunoprecipitation (RIP) assay. Xenotransplantation experiments using BALB/C nude mice were used to confirm the function of circ_0061395 in vivo. Circ_0061395 and SPOCK1 were significantly expressed in liver cancer tissues and cells. Silencing circ_0061395 reduced the proliferation, migration, invasion, tube formation and tumor spheroid formation rate of Huh-7 and SNU-387 cells. MiR-1182 was a target of circ_0061395. Silencing circ_0061395 inhibited the malignant behavior of HCC cells by releasing miR-1182. In addition, SPOCK1 was the target of miR-1182. Overexpression of SPOCK1 partially restored the inhibitory effect of miR-1182 on cell proliferation. Animal experiments confirmed the anti-tumor effect of silence circ_0061395. Circ_0061395 induced the changes of the expression of SPOCK1 by regulating miR-1182, thereby mediating the process of HCC, and at least partially promoting the development of HCC cells, providing a novel targeted therapy for HCC.

CircCAMSAP1 promotes non-small cell lung cancer proliferation and inhibits cell apoptosis by sponging miR-1182 and regulating BIRC5.

Recently, various studies have suggested that circular RNAs (circRNAs) are ubiquitous in various malignant events, including non-small cell lung cancer (NSCLC) and are closely related to cell proliferation and apoptosis. Unfortunately, the molecular functions involved in this action still have little overlap. Therefore, this study aimed to identify a novel circCAMSAP1 role in NSCLC. Overexpression of circCAMSAP1 has been demonstrated in NSCLC lung tissues and cell lines. Sequencing and RNase R experiments were planned to determine whether circCAMSAP1 is looped and exists in NSCLC. We also found that downregulated circCAMSAP1 repressed cell proliferation and increased apoptosis of NSCLC cells in vitro and suppressed xenograft tumor growth in vivo. Furthermore, a luciferase assay revealed that circCAMSAP1 could regulate baculoviral inhibitor of apoptosis protein (IAP) repeat containing 5 (BIRC5, also known as survivin) expression by directly binding to miR-1182. However, BIRC5 without 3' untranslated regions (3'UTR) could reverse the influence of downregulated circCAMSAP1 on proliferation and apoptosis in NSCLC. Together, our findings reveal a novel mechanism by which the circCAMSAP1/miR-1182/BIRC5 axis promotes NSCLC progression.

LINC01207 promotes prostate cancer progression by sponging miR-1182 to upregulate AKT3.

Prostate cancer (PC) is recognized as a common malignancy in male patients. Long non-coding RNA (lncRNA) has been implicated in the development of PC. Recently, long intergenic non-protein coding RNA 1207 (LINC01207) has been reported to regulate the carcinogenesis of multiple cancer types. However, its role in the progression of PC remains to be determined. The aim of the present study was to investigate the expression profile, clinicopathological implication and molecular mechanism of action of LINC01207 in the progression of PC. LINC01207 expression levels were compared between PC tumor and paired normal tissue samples from The Cancer Genome Atlas. The expression of LINC01207 was further analyzed in PC cell lines and a normal prostatic cell line. The role of LINC01207 in proliferation, migration and invasion of PC cells was examined using small interfering RNA-mediated silencing. Western blot analysis was used to investigate the changes in protein levels underlying the mechanism of action of LINC01207. The role of LINC01207 in tumorigenesis was evaluated in a xenograft model. LINC01207 was upregulated in PC tumor samples from TCGA data compared with paired normal tissue. LINC01207 expression was significantly increased in PC cells and tumor tissues compared with in normal prostate cells (RWPE1) and normal prostate tissues, respectively. Furthermore, LINC01207 silencing inhibited PC cell proliferation and colony formation and induced apoptosis. Mechanistic experiments showed that LINC01207 promoted carcinogenesis by sponging miR-1182 to regulate the protein levels of AKT3 in PC cell lines. Thus, the findings of the present study indicated that LINC01207 might play a role in the tumorigenesis of PC and may serve as a therapeutic target for PC treatment.

Circ_MUC16 attenuates the effects of Propofol to promote the aggressive behaviors of ovarian cancer by mediating the miR-1182/S100B signaling pathway.

BACKGROUND: Propofol is commonly used for anesthesia during surgery and has been demonstrated to inhibit cancer development, which is shown to be associated with deregulation of non-coding RNAs (ncRNAs). The objective of this study was to explore the role of circular RNA mucin 16 (circ_MUC16) in Propofol-mediated inhibition of ovarian cancer. METHODS: The expression of circ_MUC16, microRNA-1182 (miR-1182) and S100 calcium-binding protein B (S100B) mRNA was measured by quantitative real-time polymerase chain reaction (qPCR). The expression of S100B protein was checked by western blot. Cell proliferation was assessed by 3-(4, 5-di methyl thiazol-2-yl)-2, 5-di phenyl tetrazolium bromide (MTT) assay and colony formation assay. Glycolysis metabolism was assessed by glucose consumption, lactate production and ATP level. Cell migration and cell invasion were assessed by transwell assay. Cell migration was also assessed by wound healing assay. Animal study was conducted in nude mice to determine the role of circ_MUC16 in vivo. The relationship between miR-1182 and circ_MUC16 or S100B was validated by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. RESULTS: Propofol inhibited ovarian cancer cell proliferation, glycolysis metabolism, migration and invasion, which were partly recovered by circ_MUC16 overexpression. Circ_MUC16 was downregulated in Propofol-treated ovarian cancer cells. Besides, circ_MUC16 knockdown enhanced the effects of Propofol to further inhibit tumor growth in vivo. MiR-1182 was a target of circ_MUC16, and circ_MUC16 knockdown-inhibited cell proliferation, glycolysis metabolism, migration and invasion were partly restored by miR-1182 inhibition. In addition, S100B was a target of miR-1182, and miR-1182-suppressed cell proliferation, glycolysis metabolism, migration and invasion were partly restored by S100B overexpression. CONCLUSION: Circ_MUC16 overexpression alleviated the effects of Propofol to promote the aggressive behaviors of ovarian cancer by targeting the miR-1182/S100B network.

A Novel Circular RNA circCSPP1 Promotes Liver Cancer Progression by Sponging miR-1182.

INTRODUCTION: Aberrant circular RNA (circRNA) expression has been extensively discovered for its involvement in both the initiation and progression of various cancers. Through screening circRNA profile, we identified a novel circRNA has_circ_0001806, which is termed as circCSPP1 in liver cancer. In the present study, we aim to investigate the role of circCSPP1 in the progression of liver cancer. METHODS: Fluorescence in situ hybridization (FISH) was used to detect the location of circCSPP1. Function studies including MTT, colony formation assay, transwell assay and flow cytometry were carried out to detect the malignant behaviour of circCSPP1 on liver cancer cells. Luciferase assay and RNA pull down were used to detect the interaction between miR-1182 and circCSPP1 as well as RAB15. Quantitative realtime (qPCR) and Western blot were performed to evaluate the RNA and protein expression, respectively. RESULTS: CircCSPP1 knockdown inhibited the proliferation, migration and invasion while promoted apoptosis of liver cancer cells. Mechanically, we predicted and verified the target miR of circCSPP1 which is miR-1182. miR-1182 was capable of reversing the effect of circCSPP1 on liver cancer cells. Moreover, miR-1182 was found to also target RAB15 to participate in the regulation of cell phenotype. DISCUSSION: Taken together, circCSPP1 promoted progression of liver cancer cells via sponging miR-1182 which may serve as a novel prognostic and therapeutic target for liver cancer.

Exosomal Circ-XIAP Promotes Docetaxel Resistance in Prostate Cancer by Regulating miR-1182/TPD52 Axis.

BACKGROUND: Exosomal circular RNAs (circRNAs) are involved in the pathogenesis of prostate cancer (PCa) and chemotherapy resistance. This research aimed to explore the function and molecular mechanism of circRNA X-linked inhibitor of apoptosis (circ-XIAP) in docetaxel (DTX) resistance of PCa. METHODS: The expression of circ-XIAP, microRNA-1182 (miR-1182), tumor protein D52 (TPD52) was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Exosomes were detected with transmission electron microscopy (TEM). Cluster of differentiation 63 (CD63), cluster of differentiation 9 (CD9) and TPD52 protein levels were detected by Western blot (WB). FIfty percent inhibitory concentration (IC50) of DTX and cell viability were determined using Cell Counting Kit-8 (CCK-8) assay. Colony formation assay was applied to assess colony-forming ability. Cell cycle distribution and apoptosis were analyzed by flow cytometry. Transwell assay was used for measuring cell migration and invasion. Dual-reporter luciferase assay was performed to confirm the interaction between miR-1182 and circ-XIAP or TPD52. The role of circ-XIAP in vivo was confirmed via the mice xenograft model. RESULTS: Circ-XIAP and TPD52 were upregulated and miR-1182 was downregulated in DTX-resistant PCa tissue specimens and cell lines. Circ-XIAP was also overexpressed in exosomes from DTX-resistant cells and could be transmitted via exosomes. Circ-XIAP knockdown enhanced DTX sensitivity by suppressing DTX-resistant cell proliferation, migration and invasion and inducing cell cycle arrest and apoptosis. Circ-XIAP directly targeted miR-1182, and the effects of circ-XIAP knockdown were reversed by downregulating miR-1182 in DTX-resistant cells. TPD52 was the target of miR-1182, and its upregulation weakened the promotive effect of miR-1182 on DTX sensitivity. Importantly, circ-XIAP depletion inhibited tumor growth and increased DTX sensitivity in vivo. CONCLUSION: Exosomal circ-XIAP promoted DTX resistance of PCa by regulating miR-1182/TPD52 axis, providing a promising therapeutic target for PCa chemotherapy.

Circ_0001806 Promotes the Proliferation, Migration and Invasion of NSCLC Cells Through miR-1182/NOVA2 Axis.

BACKGROUND: Circular RNAs (circRNAs) are non-coding RNAs with a covalently closed loop. circRNAs affect the progression of diverse cancers. Nonetheless, circ_0001806 expression and function in non-small cell lung cancer (NSCLC) are undefined. METHODS: qRT-PCR was executed to examine circ_0001806, miR-1182 and NOVA2 mRNA expression levels in NSCLC tissues and cells. CCK-8, EdU, cell scratch test and Transwell assay were conducted to examine the viability, multiplication, migration and invasion of NSCLC cell lines H1650 and HCC827. The binding sites between circ_0001806 and miR-1182, miR-1182 and NOVA2 mRNA were predicted by the circular RNA Interactome and TargetScan databases, and the dual-luciferase reporter gene experiment was employed for verification. Western blot was implemented to examine NOVA2 expression. RESULTS: Circ_0001806 expression in NSCLC tissues and cell lines was substantially augmented, while miR-1182 expression was markedly decreased. Circ_0001806 facilitated the multiplication, migration and invasion of H1650 and HCC827 cells, while miR-1182 exerted the opposite effect. Circ_0001806 indirectly enhanced NOVA2 expression by specifically down-modulating miR-1182. CONCLUSION: Circ_0001806 augments NOVA2 expression by targeting miR-1182 to enhance the multiplication, migration and invasion of NSCLC cells.

Circ_0105346 Knockdown Inhibits Osteosarcoma Development via Regulating miR-1182/WNT7B Axis.

BACKGROUND: Osteosarcoma (OS) is a common bone malignancy in children and adolescents. Circular RNAs (circRNAs) have been reported to affect OS progression. This paper mainly delineated the role of circRNA circ_0105346 in OS development and the potential mechanism. METHODS: Quantitative reverse transcription PCR (qRT-PCR) and Western blot assays were applied to detect the expression of circ_0105346, microRNA (miR)-1182 and wingless-type MMTV integration site family 7B (WNT7B). 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay was conducted to evaluate cell viability, and flow cytometry was performed to monitor cell apoptosis and cycle. In addition, cell migration and invasion were determined via transwell assay. Wound healing assay was also employed to evaluate the migrated capacity of OS cells. Western blot assay was also employed to examine the levels of protein markers. Additionally, the interaction between miR-1182 and circ_0105346 or WNT7B was confirmed by the dual-luciferase reporter, RNA immunoprecipitation (RIP) and pull-down assays. Mouse xenograft model was constructed to clarify the effect of circ_0105346 on tumor growth in vivo. RESULTS: Circ_0105346 and WNT7B were upregulated, while miR-1182 was downregulated in OS tissues and cells. Circ_0105346 knockdown suppressed OS cell proliferation, cell cycle, migration, invasion and glycolysis, as well as accelerated apoptosis, which was attenuated by miR-1182 inhibition. Interestingly, circ_0105346 targeted miR-1182, and miR-1182 interacted with WNT7B. Circ_0105346 could upregulate WNT7B by downregulating miR-1182 expression. Furthermore, circ_0105346 knockdown blocked tumor growth in vivo. CONCLUSION: Circ_0105346 knockdown repressed OS progression by regulating miR-1182/WNT7B axis, at least in part.

Circ_0000376, a Novel circRNA, Promotes the Progression of Non-Small Cell Lung Cancer Through Regulating the miR-1182/NOVA2 Network.

BACKGROUND: Hypoxia has been shown to induce the malignant progression of cancer, including non-small cell lung cancer (NSCLC). Circular RNA (circRNA) is considered to be an important regulator of cancer progression. However, the role of a newly discovered circRNA, circ_0000376, in the progression of NSCLC is unclear. METHODS: The relative expression levels of circ_0000376, miR-1182 and neuro-oncological ventral antigen 2 (NOVA2) were detected via quantitative real-time polymerase chain reaction (qRT-PCR). Glucose consumption and lactate production were determined using Glucose Assay Kit and Lactate Assay Kit, respectively. Moreover, the protein levels of glycolysis markers and NOVA2 were measured using Western blot (WB) analysis. Furthermore, 3-(4, 5-dimethyl-2 thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay was performed to assess cell viability, and transwell assay was employed to evaluate cell migration and invasion. The interaction between miR-1182 and circ_0000376 or NOVA2 was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. In addition, animal experiments were conducted to assess the influence of circ_0000376 silencing on NSCLC tumor growth in vivo. RESULTS: Circ_0000376 was upregulated in NSCLC, and its high expression was related to the poor overall survival of NSCLC patients. Hypoxia could enhance circ_0000376 expression and promote the glycolysis, viability, migration, and invasion of NSCLC cells. However, silencing of circ_0000376 could inhibit the glycolysis, viability, migration, and invasion of hypoxia-induced NSCLC cells. Additionally, circ_0000376 could sponge miR-1182, and miR-1182 could target NOVA2. MiR-1182 silencing could reverse the inhibitory effect of circ_0000376 knockdown on NSCLC progression, and NOVA2 overexpression also could reverse the suppressive effect of miR-1182 overexpression on NSCLC progression. Meanwhile, miR-1182 inhibitor could invert the negative regulation effect of circ_0000376 silencing on NOVA2 expression. In addition, circ_0000376 knockdown inhibited the NSCLC tumor growth via regulating the miR-1182 and NOVA2 expression in vivo. CONCLUSION: Circ_0000376 promoted NSCLC progression by regulating the miR-1182/NOVA2 axis, suggesting that circ_0000376 might be a potential biomarker for NSCLC treatment.

Circ_0067934 promotes non-small cell lung cancer development by regulating miR-1182/KLF8 axis and activating Wnt/ß-catenin pathway.

Non-small cell lung cancer (NSCLC) is the primary subtype of lung cancer with high mortality. Circular RNAs (circRNAs) play a crucial role in tumor development and progression. This study aimed to explore the function of circ_0067934 in NSCLC progression and its molecular basis. The levels of circ_0067934, miR-1182 and kruppel like factor 8 (KLF8) were measured by quantitative real-time polymerase chain reaction or western blot assay. Cell viability was detected by Cell Counting Kit-8 (CCK-8) assay. Cell migration and invasion were assessed by transwell assay. Cell apoptosis was monitored by flow cytometry. The protein levels of epithelial-to-mesenchymal transition (EMT)-related markers and Wnt/ß-catenin pathway-related proteins were examined by western blot. Dual-luciferase reporter assay, RNA Immunoprecipitation (RIP) assay or RNA pull-down assay was performed to verify the interaction among circ_0067934, miR-1182 and KLF8. Xenograft assay was used to detect tumor growth in vivo. We found that circ_0067934 and KLF8 were up-regulated, while miR-1182 was down-regulated in NSCLC tissues and cells. Circ_0067934 knockdown blocked proliferation, migration, invasion and EMT and induced apoptosis in NSCLC cells. Circ_0067934 regulated NSCLC progression by sponging miR-1182. MiR-1182 targeted KLF8 to hinder NSCLC development. In addition, depletion of circ_0067934 restrained tumor growth in vivo. In conclusion, Circ_0067934 acted as a competing endogenous RNA to facilitate NSCLC progression by regulating the miR-1182/KLF8 axis and activating Wnt/ß-catenin pathway.

LINC00339 promotes growth and invasiveness of hepatocellular carcinoma by the miR-1182/SKA1 pathway.

Background: Extensive research has shown that long noncoding RNA (lncRNA) is involved in tumorigenesis, including hepatocellular carcinoma (HCC). The lncRNA LINC00339 was reported to regulate the development of lung cancer or breast cancer. However, whether LINC00339 participates in HCC progression remains unclear. Here, our results showed that LINC00339 was upregulated in HCC. Methods: qRT-PCR and in situ hybridization (ISH) was used to analyze LINC00339 expression in tumor tissues and cell lines. CCK8 and colony formation assays were used to analyze cell proliferation. Transwell assay was used to analyze cell migration and invasion. Xenograft experiment was used to test tumor growth in vivo. Results: LINC00339 overexpression was correlated with an advanced stage, metastasis, and bad prognosis in HCC patients. Functional investigation showed that LINC00339 knockdown significantly suppressed HCC cell proliferation, migration, and invasion. Moreover, decreased LINC00339 expression inhibited HCC growth in vivo. Mechanistically, LINC00339 could interact with miR-1182 to promote SKA1 expression. We also demonstrated that SKA1 acted as an oncogene and SKA1 upregulation reversed the effect of LINC00339 silencing. Conclusion: Our results illustrated that the LINC00339/miR-1182/SKA1 axis plays an essential role in HCC progression.

Enhanced expression of circ_0000735 forecasts clinical severity in NSCLC and promotes cell progression via sponging miR-1179 and miR-1182.

Although numerous dysregulated circular RNAs (circRNAs) was discovered, the study between circRNAs and non-small cell lung cancer (NSCLC) is just beginning. Here, we investigated the functions and provided a possible mechanism of circ_0000735 for NSCLC. Real-time PCR was used to elucidate the level of circ_0000735 in NSCLC tissue samples and cells. CCK8, colony formation, flow cytometric, and transwell experiments were carried out to evaluate cell proliferation, apoptosis, migratory and invasive abilities in NSCLC cell lines. Luciferase reporter assays were conducted to elucidate the mechanisms of circ_0000735 in NSCLC. Circ_0000735 was elevated in both NSCLC tissues and cells. This upregulation of circ_0000735 is associated with more advanced TNM stages and lymph node invasion. Gain and loss of function experiments documented that circ_0000735 significantly facilitated cell proliferation, migratory and invasive abilities and inhibit cell apoptosis. Moreover, we proved circ_0000735 could bound to miR-1179/1182 to exert its biological functions in NSCLC cells. Taken together, this work provided a possible treatment target for this devastating disease.

TCF3-activated LINC00152 exerts oncogenic role in osteosarcoma through regulating miR-1182/CDK14 axis.

Long noncoding RNAs (lncRNAs) have been reported to participate in tumorigenesis and diverse cellular processes in osteosarcoma (OS). However, the role of lncRNA LINC00152 in OS remains elusive. In this study, LINC00152 was highly expressed in osteosarcoma tissues and cell lines. Moreover, MTT and colony formation assays revealed that knockdown of LINC00152 significantly suppressed cell proliferation. The inhibitory effect of LINC00152 knockdown on OS cell migration and invasion was analyzed and demonstrated by transwell assays. Additionally, Chromatin immunoprecipitation (ChIP) and luciferase reporter assays suggested that LINC00152 was transcriptionally activated by the transcription factor TCF3. More importantly, mechanism investigation revealed that LINC00152 was predominantly located in the cytoplasm of OS cells and acted as a competing endogenous RNA (ceRNA) in OS by regulating miR-1182/CDK14 axis. Collectively, LINC00152 was activated by TCF3 and promotes cell proliferation and migration in osteosarcoma via miR-1182-CDK14 axis.

miR-1182 inhibits growth and mediates the chemosensitivity of bladder cancer by targeting hTERT.

microRNAs (miRNAs) have been demonstrated to contribute to tumor progression and metastasis and proposed to be key regulators of diverse biological processes. In this study, we report that miR-1182 is deregulated in bladder cancer tissues and cell lines. To characterize the role of miR-1182 in bladder cancer cells, we performed functional assays. The overexpression of miR-1182 significantly inhibits bladder cancer cell proliferation, colony formation, and invasion. Moreover, its up-regulation induced cell cycle arrest and apoptosis and mediated chemosensitivity to cisplatin in bladder cancer. Furthermore, a luciferase reporter assay and a rescue experiment indicated that miR-1182 directly targets hTERT by binding its 3'UTR. In conclusion, these results demonstrate that miR-1182 acts as a tumor suppressor and may be a potential biomarker for bladder cancer diagnosis and treatment.

miR-1182 attenuates gastric cancer proliferation and metastasis by targeting the open reading frame of hTERT.

In humans, telomerase reverse transcriptase (hTERT) determines the activity of telomerase. hTERT is an ideal anticancer target because it is universally expressed in cancer cells and plays a crucial role in carcinogenesis. In this study, we report the miR-1182-mediated post-transcriptional regulation of hTERT. Over-expression of miR-1182 in different gastric cancer cells decreased hTERT protein levels. Bioinformation and dual-luciferase assays revealed that miR-1182 modulated hTERT by binding to its open reading frame (ORF), and this miRNA recognizes elements in the nucleotide region between 2695 and 2719 of hTERT mRNA. Over-expression of hTERT by transfecting pIRES2-hTERT into U2OS cells was abolished by miR-1182, while pIRES2-hTERT-MT, in which miR-1182 target site was synonymously mutated, failed to respond to miR-1182. Further investigation revealed that miR-1182 inhibited gastric cancer proliferation and migration by targeting the ORF1 of hTERT. We also found that miR-1182 could attenuate the proliferative and metastatic potential of SGC-7901 cell in vivo. Moreover, we found a statistically significant inverse correlation between miR-1182 and hTERT protein levels in tissues from 42 gastric cancer patients. These data indicate that miR-1182 suppresses TERT, and thus it could be an effective target for the treatment of gastric cancer.