• BRAF mutation
• Melanoma
• NcRNAs
• Resistance
• V600E mutation

• Humans
• Melanoma/genetics
• Melanoma/drug therapy
• Melanoma/pathology
• Proto-Oncogene Proteins B-raf/genetics
• Mutation
• RNA, Untranslated/genetics
• Skin Neoplasms/genetics
• Skin Neoplasms/drug therapy
• Skin Neoplasms/pathology
• Animals
• Drug Resistance, Neoplasm/genetics
• MicroRNAs/genetics
• Molecular Targeted Therapy
• RNA, Long Noncoding/genetics

• University of Haöil University of Hail

• SUMO1P3
• bladder cancer progression
• liquid biopsy
• long non-coding RNA
• urinary biomarker

• breast cancer
• cell cycle
• lncRNAs

• Humans
• Female
• Breast Neoplasms/genetics
• Breast Neoplasms/therapy
• Breast Neoplasms/pathology
• RNA, Long Noncoding/genetics
• RNA, Long Noncoding/metabolism
• Cell Cycle/genetics
• Transcriptome
• Oncogenes

• Gene delivery
• Melanoma
• Nanomedicine
• Nanovectors
• Targeted therapy

• AMT/T
• Aging
• Artificial mitochondrial transfer / transplant
• Gene editing
• Mitochondria
• Skin
• lncRNAs

• Humans
• RNA, Long Noncoding/genetics
• Skin Aging/genetics
• Aging, Premature/metabolism
• Neoplasms/genetics
• Mitochondria/genetics
• Mitochondria/metabolism

• R21 OD031970 NIH HHS

• Immune microenvironment
• Immunotherapy response
• Melanoma
• Prognostic models
• lncRNA

• Biomarker
• Diagnosis
• Long non-coding RNAs
• Melanoma
• Therapy

• immunotherapy
• lncRNAs
• melanoma
• targeted therapy
• tumor microenvironment

• Chemoresistance
• FOXM1
• Gastric cancer
• Thiostrepton (THIO)
• Tumor growth and metastasis

• Animals
• Humans
• Mice
• Apoptosis
• Cell Line, Tumor
• Cell Proliferation
• Forkhead Box Protein M1/genetics
• Forkhead Box Protein M1/metabolism
• Gene Expression Regulation, Neoplastic
• Reactive Oxygen Species/metabolism
• Stomach Neoplasms/drug therapy
• Stomach Neoplasms/genetics
• Stomach Neoplasms/metabolism
• Thiostrepton/pharmacology
• Thiostrepton/therapeutic use

Invasion and metastasis of melanoma are a series of complicated biological events regulated by multiple factors. The coregulation of many molecules involved in the development and progression of melanoma contributes to invasion and migration. mGluR1 is a metabotropic glutamate receptor that is overexpressed in melanocytes and is sufficient to induce melanoma. In our study, we found that mGluR1 was obviously increased in melanoma. Furthermore, we found that miR-129-5p could directly target and regulate mGluR1 mRNA, which was significantly reduced in A375 cells. Overexpression of miR-129-5p inhibited cell migration, invasion and clonal formation. lncRNA-AC130710 directly targeted and suppressed miR-129-5p in A375 cells. Downregulation of lncRNA-AC130710 suppressed the levels of mGluR1 mRNA by promoting miR-129-5p expression and further inhibiting migration, invasion and colony formation in A375 cells, which was associated with the activation of the PKCα-MAPK signaling pathway. Taken together, our study showed that the lncRNA-AC130710/miR-129-5p/mGluR1 axis plays an important role in the invasion and metastasis of melanoma.

• invasion
• lncRNA
• mGluR1
• melanoma
• migration

• drug resistance
• drug targeting
• lncRNAs
• melanoma
• metastasis
• phenotype switch

• Carcinogenesis/genetics
• Gene Expression Regulation, Neoplastic
• Humans
• Melanoma/genetics
• Melanoma/pathology
• Oncogenes
• RNA, Long Noncoding/genetics

• 20508 Italian Association for Cancer Research

• apoptosis
• cell cycle
• cellular senescence
• lncRNA

• circular RNAs
• cutaneous melanoma
• immunotherapy
• long noncoding RNAs
• targeted therapy

• Humans
• Melanoma/drug therapy
• Melanoma/therapy
• MicroRNAs/genetics
• MicroRNAs/metabolism
• RNA, Circular/genetics
• RNA, Long Noncoding/genetics
• RNA, Long Noncoding/metabolism
• Skin Neoplasms/genetics
• Skin Neoplasms/therapy

Our previous work using a melanoma progression model composed of melanocytic cells (melanocytes, primary and metastatic melanoma samples) demonstrated various deregulated genes, including a few known lncRNAs. Further analysis was conducted to discover novel lncRNAs associated with melanoma, and candidates were prioritized for their potential association with invasiveness or other metastasis‐related processes. In this sense, we found the intergenic lncRNA U73166 (ENSG00000230454) and decided to explore its effects in melanoma. For that, we silenced the lncRNA U73166 expression using shRNAs in a melanoma cell line. Next, we experimentally investigated its functions and found that migration and invasion had significantly decreased in knockdown cells, indicating an essential association of lncRNA U73166 for cancer processes. Additionally, using naïve and vemurafenib‐resistant cell lines and data from a patient before and after resistance, we found that vemurafenib‐resistant samples had a higher expression of lncRNA U73166. Also, we retrieved data from the literature that indicates lncRNA U73166 may act as a mediator of RNA processing and cell invasion, probably inducing a more aggressive phenotype. Therefore, our results suggest a relevant role of lncRNA U73166 in metastasis development. We also pointed herein the lncRNA U73166 as a new possible biomarker or target to help overcome clinical vemurafenib resistance.

• ENSG00000230454
• U73166
• invasion
• lncRNAs
• melanoma
• migration
• resistance
• vemurafenib

• Breast cancer
• drug resistance
• forkhead box transcription factor M1 (FoxM1)
• therapeutics
• tumorigenesis

• microRNA
• non-coding RNA
• skin cancer

• drug resistance
• gene regulation
• lncRNA
• melanoma
• miRNA sponging
• oncogenes
• targeted therapy
• tumor suppressors

• circRNAs
• lncRNAs
• melanoma
• microRNAs
• non-coding RNAs

Long noncoding RNAs (lncRNAs) have been reported as important molecules in cholangiocarcinoma (CCA) occurrence and development. A previous study showed that lncRNA GAS5 (GAS5) was an oncogene in some tumors. But the role of GAS5 in CCA progression reminds unclear. This research was designed to study the expression and potential effects of GAS5 in the progression of CCA.

The expression of GAS5 in CCA tissues was evaluated through mining of the TCGA and GEPIA databases. qRT-PCR was applied to validate the results in our clinical samples. χ² test was used to analyze the association between the expression level of tissue GAS5 and different clinicopathological parameters of CCA patients. The target gene of GAS5 was predicted by bioinformatic databases, and further verified by luciferase reporter assays. Finally, the role of GAS5 in CCA cells invasion and proliferation was detected by Transwell assay and CCK-8 assay.

Compared to the adjacent nontumor tissues and the normal human intrahepatic biliary epithelial cell, the expression of GAS5 was markedly increased in CCA tissues (p<0.001) and cell lines (p<0.01), respectively. CCA patients with high GAS5 expression tended to present lymph node metastasis (p<0.001) and had advanced clinical stage (p=0.006). The bioinformatics analysis predicted that hsa-miR-1297 was the potential target gene of GAS5, which was validated by luciferase reporter assays. In addition, the function study showed that GAS5 acted as a “sponge” to downregulate hsa-miR-1297, thus modulating CCA cell proliferation and invasion.

GAS5 acts as an endogenous sponge of hsa-miR-1297 to promote CCA cell proliferation and invasion, which might be a potential biomarker and therapeutic target for CCA.

• GAS5
• invasion
• metastasis
• miR-1297
• proliferation

Gallbladder cancer (GBC) is an aggressive type of biliary tract cancer that lacks effective therapeutic targets. Fork head box M1 (FoxM1) is an emerging molecular target associated with tumor progression in GBC, and accumulating evidence suggests that vascular endothelial growth factor (VEGF) promotes various tumors by inducing neoangiogenesis.

To investigate the role of FoxM1 and the angiogenesis effects of VEGF-A in primary GBC.

Using immunohistochemistry, we investigated FoxM1 and VEGF-A expression in GBC tissues, paracarcinoma tissues and cholecystitis tissues. Soft agar, cell invasion, migration and apoptosis assays were used to analyze the malignant phenotype influenced by FoxM1 in GBC. Kaplan-Meier survival analysis was performed to evaluate the impact of FoxM1 and VEGF-A expression in GBC patients. We investigated the relationship between FoxM1 and VEGF-A by regulating the level of FoxM1. Next, we performed MTT assays and Transwell invasion assays by knocking out or overexpressing VEGF-A to evaluate its function in GBC cells. The luciferase assay was used to reveal the relationship between FoxM1 and VEGF-A. BALB/c nude mice were used to establish the xenograft tumor model.

FoxM1 expression was higher in GBC tissues than in paracarcinoma tissues. Furthermore, the high expression of Foxm1 in GBC was significantly correlated with a malignant phenotype and worse overall survival. Meanwhile, high expression of FoxM1 influenced angiogenesis; high expression of FoxM1 combined with high expression of VEGF-A was related to poor prognosis. Attenuated FoxM1 significantly suppressed cell proliferation, transfer and invasion in vitro. Knockdown of FoxM1 in GBC cells reduced the expression of VEGF-A. Luciferase assay showed that FoxM1 was the transcription factor of VEGF-A, and knockdown VEGF-A in FoxM1 overexpressed cells could partly reverse the malignancy phenotype of GBC cells. In this study, we found that FoxM1 was involved in regulation of VEGF-A expression.

FoxM1 and VEGF-A overexpression were associated with the prognosis of GBC patients. FoxM1 regulated VEGF-A expression, which played an important role in the progression of GBC.

• Gallbladder neoplasms
• Fork head box M1
• Vascular endothelial growth factor-A
• Angiogenesis
• Progression
• Prognosis

• Animals
• Cell Line, Tumor
• Cell Movement
• Cell Proliferation
• Forkhead Box Protein M1/genetics
• Gallbladder Neoplasms/genetics
• Gene Expression Regulation, Neoplastic
• Humans
• Mice
• Mice, Inbred BALB C
• Mice, Nude
• Vascular Endothelial Growth Factor A

Forkhead box transcription factor, FOXM1 is implicated in several cellular processes such as proliferation, cell cycle progression, cell differentiation, DNA damage repair, tissue homeostasis, angiogenesis, apoptosis, and redox signaling. In addition to being a boon for the normal functioning of a cell, FOXM1 turns out to be a bane by manifesting in several disease scenarios including cancer. It has been given an oncogenic status based on several evidences indicating its role in tumor development and progression. FOXM1 is highly expressed in several cancers and has also been implicated in poor prognosis. A comprehensive understanding of various aspects of this molecule has revealed its role in angiogenesis, invasion, migration, self- renewal and drug resistance. In this review, we attempt to understand various mechanisms underlying FOXM1 gene and protein regulation in cancer including the different signaling pathways, post-transcriptional and post-translational modifications. Identifying crucial molecules associated with these processes can aid in the development of potential pharmacological approaches to curb FOXM1 mediated tumorigenesis.

• FOXM1
• cell signaling
• miRNA
• post-transcriptional regulation
• post-translational regulation

• Cancer
• Cancer metastasis
• Cancer therapy
• EMT
• LncRNA

• biomarkers
• cancer therapy
• lncRNA
• melanoma
• skin cancer

• Animals
• Biomarkers, Tumor
• Body Fluids
• Cell-Free Nucleic Acids
• Gene Expression Regulation, Neoplastic
• Humans
• Melanoma/diagnosis
• Melanoma/genetics
• Melanoma/therapy
• Mutation
• Neoplasm Staging
• Prognosis
• Proto-Oncogene Proteins B-raf/genetics
• RNA, Long Noncoding/genetics
• Skin Neoplasms/diagnosis
• Skin Neoplasms/genetics
• Skin Neoplasms/therapy
• Melanoma, Cutaneous Malignant

Cell cycle is regulated by a number of proteins namely cyclin-dependent kinases (CDKs) and their associated cyclins which bind with and activate CDKs in a phase specific manner. Additionally, several transcription factors (TFs) such as E2F and p53 and numerous signaling pathways regulate cell cycle progression. Recent studies have accentuated the role of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) in the regulation of cell cycle. Both lncRNAs and miRNAs interact with TFs participating in the regulation of cell cycle transition. Dysregulation of cell cycle regulatory miRNAs and lncRNAs results in human disorders particularly cancers. Understanding the role of lncRNAs, miRNAs, and TFs in the regulation of cell cycle would pave the way for design of anticancer therapies which intervene with the cell cycle progression. In the current review, we describe the role of lncRNAs and miRNAs in the regulation of cell cycle and their association with human malignancies.

• cell cycle
• expression
• long non coding RNA
• microRNA
• polymorphism

Rheumatoid arthritis (RA), a chronic systemic disease, is featured with inflammatory synovitis, which can lead to destruction on bone and cartilage and even cause disability. Emerging studies demonstrated that Fibroblast-like synoviocytes (FLS) is a vital cellular participant in RA progression. Long non-coding RNAs (lncRNAs) are also reported to participate in the pathogenesis of RA. In our present study, lncRNA microarray analysis was applied to screen out lncRNAs differentially expressed in RA FLS. Among which, cytoskeleton regulator RNA (LINC00152) presented biggest fold change. Gain- or loss-of function assays were further carried out in RA FLS, and the results revealed that LINC00152 promoted proliferation but induced apoptosis in RA FLS. Furthermore, up-regulation of LINC00152 may induce promotion of Wnt/β-catenin signaling pathway in RA FLS. Mechanistically, we found that forkhead box M1 (FOXM1) transcriptionally activated LINC00152 in RA FLS. Additionally, LINC00152 positively regulated FOXM1 via sponging miR-1270. In conclusion, the present study focused on elucidating the function of FOXM1/LINC00152 positive feedback loop in RA FLS and its association with Wnt/β-catenin signaling.

• FOXM1
• LINC00152
• RA FLS
• Wnt/β-catenin signaling pathway

• biomarkers
• cutaneous melanoma
• drug resistance
• immunotherapy
• invasion
• lncRNA
• metastasis
• miRNA
• targeted therapy

• Biomarker
• Melanoma
• lncRNA

• CXCL6
• E2F3
• circRNA
• circ_0005394
• hepatocellular carcinoma

• cartilage
• chondrocyte
• endogenous retrovirus
• retrotransposon
• skeletal development

• Animals
• Bone Development/genetics
• Chondrocytes/cytology
• Chondrocytes/metabolism
• Chondrogenesis/genetics
• Gene Expression Regulation, Developmental
• Humans
• Mammals
• Retroelements

• CRC
• UCA1
• ceRNA
• exosome
• long noncoding RNA
• metastasis

Long non-coding RNAs (lncRNAs) are novel regulators for post-transcriptional gene expression, and altered lncRNAs function and expression are associated with tumorigenesis and cancer progression, although the biological functions of most lncRNAs in various cancer types and their underlying regulatory interactions have remained largely elusive. Our previous study identified microRNA (miR)-181a as a regulator of Kruppel-like factor 6 (KLF6). In the present study, a bioinformatical analysis was performed to identify the novel lncRNA CR749391 as a potential regulator of miR-181a that contains four putative binding sites. Subsequent in vitro experiments in gastric cancer (GC) cells demonstrated that CR749391 interacted with miR-181a to regulate KLF6 expression. First, a direct binding interaction was confirmed using luciferase reporter and RNA immunoprecipitation and pull-down assays. In addition, CR749391 was observed to be downregulated in GC compared with that of normal gastric cell lines. A functional study also revealed that CR749391 depletion in normal gastric epithelial cells promoted cell viability, migration and invasion, and conferred resistance to apoptosis, whereas ectopic CR749391 overexpression had the opposite effect in GC cells and inhibited in vivo tumor growth. In addition, CR749391 was observed to be downregulated in GC compared with that of normal gastric tissues, which was associated with KLF6 but inversely associated with miR-181a levels. Overall, the CR749391/miR-181a regulatory interaction and association between CR749391 and KLF6 may enhance the current understanding of GC pathogenesis, although CR749391 association with GC prognosis needs further study. The current study could provide a novel approach for lncRNA-mediated targeted GC therapy.

• Kruppel-like factor 6
• gastric cancer
• long non-coding RNA
• microRNA sponge

Long noncoding RNA 00703 (LINC00703) was found originating from a region downstream of Kruppel-like factor 6 (KLF6) gene, having 2 binding sites for miR-181a. Since KLF6 has been reported as a target of miR-181a in gastric cancer (GC), this study aims to investigate whether LINC00703 regulates the miR-181a/KLF6 axis and plays a functional role in GC pathogenesis.

GC tissues, cell lines, and nude mice were included in this study. RNA binding protein immunoprecipitation (RIP) and pull-down assays were used to evaluate interaction between LINC00703 and miR-181a. Quantitative real-time polymerase chain reaction and western blot were applied for analysis of gene expression at the transcriptional and protein levels. A nude xenograft mouse model was used to determine LINC00703 function in vivo.

We revealed that LINC00703 competitively interacts with miR-181a to regulate KLF6. Overexpression of LINC00703 inhibited cell proliferation, migration/invasion, but promoted apoptosis in vitro, and arrested tumor growth in vivo. LINC00703 expression was found to be decreased in GC tissues, which was positively correlated with KLF6, but negatively with the miR-181a levels.

LINC00703 may have an anti-cancer function via modulation of the miR-181a/KLF6 axis. This study also provides a new potential diagnostic marker and therapeutic target for GC treatment.

• Gastric cancer
• KLF6
• LincRNAs
• miRNA sponge

Melanoma is a rare but fatal form of skin cancer and acral lentiginous melanoma (ALM) is one of its most common types. Long non-coding RNA (lncRNA) has emerged as a crucial molecule in the development and progression of human cancers, and several studies have revealed that lncRNAs may be associated with the pathogenesis, progression and metastasis of melanoma. To demonstrate the association between ALM and lncRNAs, microarray analysis was performed in tumor and adjacent non-tumor tissues. A total of 4,488 lncRNAs and 3,913 mRNAs were identified to be differentially expressed in these samples. Among them, 2,211 and 2,277 lncRNAs were upregulated and downregulated in the ALM samples compared with adjacent tissues, respectively. In addition, 1,191 and 2,722 mRNAs were upregulated and downregulated, respectively. Additionally, five randomly selected lncRNAs (fold-change >2; P<0.05) were validated by reverse transcription-quantitative PCR. An lncRNA and mRNA co-expression network and competing endogenous network analysis were also constructed. In summary, the results of the present study may reveal a novel mechanism associated with the pathogenesis and malignant biological processes of ALM and indicate that lncRNAs may serve as potential targets for the treatment of ALM.

• acral lentiginous melanoma
• co-expression network
• competing endogenous RNA network
• long non-coding RNA
• microarray analysis

• BRG1
• CPS1-IT1
• Cyr61
• melanoma
• metastasis

• Adult
• Cell Movement/genetics
• Cysteine-Rich Protein 61/genetics
• Cysteine-Rich Protein 61/metabolism
• DNA Helicases/genetics
• DNA Helicases/metabolism
• Epithelial-Mesenchymal Transition/genetics
• Female
• Gene Expression Regulation, Neoplastic/genetics
• Humans
• Male
• Melanoma/genetics
• Melanoma/metabolism
• Melanoma/pathology
• Middle Aged
• Neoplasm Invasiveness/genetics
• Nuclear Proteins/genetics
• Nuclear Proteins/metabolism
• RNA, Long Noncoding/genetics
• Skin Neoplasms/genetics
• Skin Neoplasms/metabolism
• Skin Neoplasms/pathology
• Transcription Factors/genetics
• Transcription Factors/metabolism
• Melanoma, Cutaneous Malignant

UCA1 (urothelial carcinoma associated 1) is a long non-coding RNA (lncRNA) that was found overexpressed in various human cancers including prostate cancer (PCa). However, the aspect of UCA1-miRNA-mRNA interaction in PCa remains unclear. In this study, we confirmed the role of UCA1 in PCa and found that UCA1 downregulation inhibited cell proliferation of PCa cells. Then we demonstrated that repressed UCA1 promoted the microRNA-143 (miR-143) expression and miR-143 could bind to the predicted binding site of UCA1. We then proved the anti-tumor role of miR-143 in PCa. Furthermore, we found that miR-143 displays its role in PCa via modulating the MYO6 expression. In summary, our study demonstrated that UCA1 exerts oncogenes activity in PCa, acting mechanistically by upregulating MYO6 expression through “sponging” miR-143.

• MYO6
• PCa
• UCA1
• ceRNA
• long noncoding RNA
• miR-143

The long non-coding RNA, urothelial carcinoma associated 1 (UCA1) has been demonstrated to play important roles in various types of cancers. This study investigated the functional role of UCA1 in glioma and explored the underlying molecular mechanisms. UCA1 was found to be highly up-regulated in glioma cells, and knock-down of UCA1 inhibited cell growth, invasion and migration, and also induced apoptosis in glioma cells. On the other hand, overexpression of UCA1 promoted cell proliferation, cell invasion and migration in glioma cells. Knock-down of UCA1 suppressed the activity of Wnt/β-catenin signaling, and treatment with lithium chloride restored the inhibitory effect of UCA1 knock-down on cell invasion and migration. More importantly, the aberrant expression of UCA1 was associated with chemo-resistance to cisplatin and temozolomide in glioma cells via interacting with Wnt/β-catenin signaling. In vivo studies showed that overexpression of UCA1 promoted the in vivo tumor growth of U87 cells in the nude mice. Clinically, UCA1 was found to be up-regulated in glioma tissues and higher expression level of UCA1 was correlated with poor survival in patients with glioma. Taken together, our results showed that UCA1 had a functional role in the regulation of glioma cell growth, invasion and migration, and chemo-resistance possibly via Wnt/β-catenin signaling pathway.

• Wnt/β-catenin
• apoptosis
• cell proliferation
• glioma
• urothelial carcinoma associated 1

• Dopaminergic neurons
• Inflammation
• Oxidative stress
• PI3K/Akt signaling pathway
• Parkinson's disease
• UCA1

• Cancer
• UCA1
• Urothelial carcinoma-associated 1
• lncRNA

• Cutaneous malignant melanoma
• LncRNA FOXD3-AS1
• MAP3K2
• miR-325

• UCA1
• cancer
• lncRNA
• mechanism
• prognostic

Melanoma is the deadliest form of skin cancer, and little is known about the impact of deregulated expression of long noncoding RNAs (lncRNAs) in the progression of this cancer. In this study, we explored RNA-Seq data to search for lncRNAs associated with melanoma progression. We found distinct lncRNA gene expression patterns across melanocytes, primary and metastatic melanoma cells. Also, we observed upregulation of the lncRNA ZEB1-AS1 (ZEB1 antisense RNA 1) in melanoma cell lines. Data analysis from The Cancer Genome Atlas (TCGA) confirmed higher ZEB1-AS1 expression in metastatic melanoma and its association with hotspot mutations in BRAF (B-Raf proto-oncogene, serine/threonine kinase) gene and RAS family genes. In addition, a positive correlation between ZEB1-AS1 and ZEB1 (zinc finger E-box binding homeobox 1) gene expression was verified in primary and metastatic melanomas. Using gene expression signatures indicative of invasive or proliferative phenotypes, we found an association between ZEB1-AS1 upregulation and a transcriptional profile for invasiveness. Enrichment analysis of correlated genes demonstrated cancer genes and pathways associated with ZEB1-AS1. We suggest that the lncRNA ZEB1-AS1 could function by activating ZEB1 gene expression, thereby influencing invasiveness and phenotype switching in melanoma, an epithelial-to-mesenchymal transition (EMT)-like process, which the ZEB1 gene has an essential role.

• UCA1
• cancer
• drug resistance
• invasion
• metabolism
• micro RNA
• proliferation

The aim of this study was to explore the roles of the long noncoding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) on cisplatin resistance in ovarian cancer and the underlying mechanisms. We investigated the expression of lncRNAs in 3 paired cisplatin-sensitive and cisplatin-resistant tissues of ovarian cancer by microarray analysis. The qRT-PCR analysis was to investigate the expression pattern of UCA1 in cisplatin-resistant ovarian cancer patient tissues and cell lines. Then we examined the effects of UCA1 on cisplatin resistance in vitro and in vivo. In this study, UCA1 was observed to be upregulated in cisplatin-resistant patient tissues and cell lines. Knockdown of UCA1 inhibited cell proliferation and promoted the cisplatin-induced cell apoptosis in ovarian cancer cells. Then we demonstrated that repressed UCA1 promoted the miR-143 expression and miR-143 could bind to the predicted binding site of UCA1. Furthermore, we found that miR-143 displayed its role via modulating the FOSL2 expression. Importantly, we demonstrated that UCA1 was upregulated in serum exosomes from cisplatin-resistant patients. In summary, our study demonstrated that UCA1 modulates cisplatin resistance through the miR-143/FOSL2 pathway in ovarian cancer.

• UCA1
• ceRNA
• cisplatin
• lncRNA
• miR-143
• ovarian cancer