A SOX9‐AS1/miR‐5590‐3p/SOX9 positive feedback loop drives tumor growth and metastasis in hepatocellular carcinoma through the Wnt/β‐catenin pathway

Zhang, Wei; Wu, Yanhui; Hou, Bingwu; Wang, Yadong; Deng, Dongfeng; Fu, Zhihao; Xu, Zongquan

doi:10.1002/1878-0261.12560

Cited by 51 publications

(43 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, down-regulation of lncRNA ZEB1-AS1 suppresses the proliferation and invasion in OSCC by inhibiting ZEB1 [41]. LncRNA SOX9-AS1 positively regulates SOX9 in hepatocellular carcinoma and drives tumor growth [42]. Here, we examined the level of TMPO mRNA in cells transfected with TMPO-AS1-specific shRNAs and identified that TMPO-AS1 positively regulated TMPO in TC cells.…”

Section: Discussionmentioning

confidence: 98%

TMPO-AS1 promotes cell proliferation of thyroid cancer via sponging miR-498 to modulate TMPO

Feng

Zhang

et al. 2020

Cancer Cell Int

View full text Add to dashboard Cite

Background: Thyroid cancer (TC) is the most frequent endocrine malignancy. Long noncoding RNAs (lncRNAs) have been confirmed to act as significant roles in tumor development. The role of lncRNA TMPO-AS1 in TC is still unclear, so it remains to be explored. The aim of the research is to investigate the role and regulatory mechanism of TMPO-AS1 in TC. Methods: TMPO-AS1 and TMPO expression in TC tumors and cells was detected by TCGA database and QRT-PCR assay respectively. CCK-8, EDU, TUNEL and western blot assays were conducted to identify the biological functions of TMPO-AS1 in TC. Luciferase reporter and RNA pull down assays were conducted to measure the interaction among TMPO-AS1, TMPO and miR-498. Results: TMPO-AS1 was overexpressed in TC tissues and cell lines. Knockdown of TMPO-AS1 suppressed cell growth and accelerated cell apoptosis in TC. Furthermore, downregulation of TMPO-AS1 suppressed TMPO expression in TC. The data suggested that TMPO expression was upregulated in TC tissues and cell lines and was positively correlated with TMPO-AS1 expression in TC. Furthermore, the expression of miR-498 presented low expression in TC cells. And miR-498 expression was negatively regulated by TMPO-AS1, meanwhile, TMPO expression was negatively regulated by miR-498 in TC cells. Besides, it was confirmed that TMPO-AS1 could bind with miR-498 and TMPO in TC cells. In addition, it was validated that TMPO-AS1 elevated the levels of TMPO via sponging miR-498 in TC cells. Conclusions: TMPO-AS1 promotes cell proliferation in TC via sponging miR-498 to modulate TMPO.

show abstract

Section: Discussionmentioning

confidence: 98%

TMPO-AS1 promotes cell proliferation of thyroid cancer via sponging miR-498 to modulate TMPO

Feng

Zhang

et al. 2020

Cancer Cell Int

View full text Add to dashboard Cite

show abstract

“…Previous study demonstrated that lncRNA SNHG14 sponged miR-5590-3p to promote prostate cancer malignancy [34]. LncRNA SOX9-AS1 axis could play regulatory role in metastasis in hepatocellular carcinoma by targeting miR-5590-3p to regulate Wnt/β-catenin pathway [17]. SNHG14 and SOX9-AS1 in TNBC may also affect cell function by targeting miR-5590-3p.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have shown that miR-5590-3p is also involved in the regulation of cancer, being able to inhibit diffuse large B cell lymphoma progression and immune evasion [16]. In addition, it can also regulate tumour growth and metastasis in hepatocellular carcinoma through the Wnt/β-catenin pathway [17]. In particular, miR-5590-3p is downregulated in TNBC [18].…”

mentioning

confidence: 99%

Long non-coding RNA MIR100HG promotes the migration, invasion and proliferation of triple-negative breast cancer cells by targeting the miR-5590-3p/OTX1 axis

et al. 2020

View full text Add to dashboard Cite

Background As an aggressive subtype of breast cancer with a high risk of recurrence, triple-negative breast cancer (TNBC) lacks available treatment targets. LncRNA MIR100HG promotes cell proliferation in TNBC. However, few studies have investigated the molecular mechanism of MIR100HG in TNBC. Thus, additional in-depth investigations are needed to unravel its associated regulatory mechanism. Methods MIR100HG and miR-5590-3p expression in TNBC tissue samples and cell lines was detected by RT-qPCR. Flow cytometry, transwell, wound-healing, CCK8 and colony formation assays were performed to analyse cell apoptosis, cell cycle, invasion, migration and proliferation. The protein expression of orthodenticle homeobox 1 (OTX1) and proteins in the ERK/MAPK signalling pathway were assessed by western blot analysis. Bioinformatics and luciferase assay were performed to predict and validate the interaction between MIR100HG and miR-5590-3p as well as OTX1 and miR-5590-3p. RNA immunoprecipitation (RIP) was used to detect the interaction between MIR100HG and miR-5590-3p. Subcutaneous tumour growth was observed in nude mice. Immunohistochemistry (IHC) analysis was used to assess OTX1 expression in tumour tissues. Results MIR100HG expression was upregulated, whereas that of miR-5590-3p was downregulated in TNBC. MIR100HG was shown to directly interact with miR-5590-3p. Furthermore, MIR100HG knockdown could promote TNBC cell apoptosis and cell cycle arrest in G0/G1 phase while inhibiting migration, invasion and proliferation. Furthermore, miR-5590-3p inhibition showed the opposite results and could reverse the effect of MIR100HG knockdown in TNBC cells. MiR-5590-3p downregulated the ERK/MAPK signalling pathway, suppressed the migration, invasion and proliferation of TNBC cells and promoted their apoptosis and cell cycle arrest in G0/G1 phase by targeting OTX1. In addition, MIR100HG knockdown inhibited OTX1 expression by upregulating miR-5590-3p in vivo, thereby inhibiting tumour growth. Conclusions MIR100HG promotes the progression of TNBC by sponging miR-5590-3p, thereby upregulating OTX1, suggesting a new potential treatment target for TNBC.

show abstract

“…Glycogen synthase kinase 3β (GSK3β) is a pivotal regulator of β-catenin signaling[ 102 ], and the lncRNA SNHG5 acts as a miR-26a-5p sponge to enhance GSK3β expression, thereby activating the Wnt/β-catenin pathway to facilitate HCC metastasis and EMT[ 103 ]. In addition, sex determining region Y-box (SOX) 9 can activate the Wnt/β-catenin pathway in HCC[ 104 ], and the lncRNA S OX9-AS1 facilitates HCC growth and metastasis by increasing SOX9 expression to activate the Wnt/β-catenin pathway by acting as a miR-5590-3p sponge[ 105 ]. In HCC, interleukin (IL)-6 is associated with the activation of Janus kinase 2 (JAK2)/STAT3 signaling[ 106 ]; cyclin-dependent kinase (CDK) 8 and low-density lipoprotein receptor-related protein 6 (LRP6) are associated with the activation of Wnt/β-catenin signaling[ 107 , 108 ], and the lncRNA DLGAP1-AS1 increases the expression of IL-6 and CDK8/LRP6 by functioning as a sponge of miR-26a-5p and miR-26b-5p, thereby activating JAK2/STAT3 and Wnt/β-catenin signaling to facilitate EMT and the progression of HCC, respectively[ 109 ].…”

Section: Role Of Lncrnas As Cernas In Hccmentioning

confidence: 99%

Role of long noncoding RNA-mediated competing endogenous RNA regulatory network in hepatocellular carcinoma

Niu¹,

Wang²,

Dong³

et al. 2020

WJG

View full text Add to dashboard Cite

Long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) are noncoding RNAs (ncRNAs) that occupy over 90% of the human genome, and their main function is to directly or indirectly regulate messenger RNA (mRNA) expression and participate in the tumorigenesis and progression of malignances. In particular, some lncRNAs can interact with miRNAs as competing endogenous RNAs (ceRNAs) to modulate mRNA expression. Accordingly, these RNA molecules are interrelated and coordinate to form a dynamic lncRNA-mediated ceRNA regulatory network. Mounting evidence has revealed that lncRNAs that act as ceRNAs are closely related to tumorigenesis. To date, numerous studies have established many different regulatory networks in hepatocellular carcinoma (HCC), and perturbations in these ceRNA interactions may result in the initiation and progression of HCC. Herein, we emphasize recent advances concerning the biological function of lncRNAs as ceRNAs in HCC, with the aim of elucidating the molecular mechanism underlying these HCC-related RNA molecules and providing novel insights into the diagnosis and treatment of HCC.

show abstract

A SOX9‐AS1/miR‐5590‐3p/SOX9 positive feedback loop drives tumor growth and metastasis in hepatocellular carcinoma through the Wnt/β‐catenin pathway

Cited by 51 publications

References 32 publications

TMPO-AS1 promotes cell proliferation of thyroid cancer via sponging miR-498 to modulate TMPO

TMPO-AS1 promotes cell proliferation of thyroid cancer via sponging miR-498 to modulate TMPO

Long non-coding RNA MIR100HG promotes the migration, invasion and proliferation of triple-negative breast cancer cells by targeting the miR-5590-3p/OTX1 axis

Role of long noncoding RNA-mediated competing endogenous RNA regulatory network in hepatocellular carcinoma

Contact Info

Product

Resources

About