Circular RNA circ_0006948 Promotes Esophageal Squamous Cell Carcinoma Progression by Regulating microRNA-3612/LASP1 Axis

Tang, Rongzhu; Zhou, Qiang; Xu, Qingmei; Lu, Ling; Zhou, Ying

doi:10.1007/s10620-021-07057-4

Cited by 11 publications

(9 citation statements)

References 40 publications

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“…[ 52 ] Interestingly, miR‐3612 expression has been identified as downregulated in ESCC, and its overexpression has shown to significantly impede cell proliferation, migration, invasion, and trigger apoptosis in TE‐1 and EC109 cells. [ 25 ] Mechanistically, lncRNA ZFPM2‐AS1 can expedite the stimulative effect on ESCC cell growth by sponging miR‐3612. [ 26 ] Consistent with these findings, our study revealed a reduction in miR‐3612 expression in EC cells and further investigations demonstrated that LINC01116 acted as a sponge for miR‐3612, repressing its expression under hypoxic conditions.…”

Section: Discussionmentioning

confidence: 99%

“…[ 23 ] Despite these findings, the specific functions and mechanisms of LINC01116 in EC remain poorly understood. Furthermore, microRNAs (miRNAs) have been implicated in essential regulatory roles in EC, [ 24 ] with miR‐3612 found to be downregulated in ESCC tissues and cells, [ 25 ] and confirmed as a tumor suppressor. [ 26 ] Intriguingly, LINC01116 has been reported to act a sponge for miR‐3612, promoting melanoma development [ 27 ] and it acts as an oncogene in bladder cancer cells by targeting the miR‐3612/ELK3 pathway to facilitate malignant characteristics.…”

Section: Introductionmentioning

confidence: 99%

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Hypoxia‐induced factor‐1α promotes radioresistance of esophageal cancer cells by transcriptionally activating LINC01116 and suppressing miR‐3612 under hypoxia

Zhang,

Wang,

et al. 2023

J Biochem & Molecular Tox

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Esophageal cancer (EC) is a challenging tumor to treat with radiotherapy, often exhibiting resistance to this treatment modality. To explore the factors influencing radioresistance, we focused on the role of hypoxia‐induced factor‐1α (HIF‐1α), and its interaction with the long noncoding RNA long intergenic nonprotein coding RNA 1116 (LINC01116). We analyzed the LINC01116 expression in EC and EC cell lines/human normal esophageal epithelial cell line (Het‐1A). LINC01116 was silenced/overexpressed in EC109/KYSE30 cells under hypoxia, followed by radioresistance assessment. We measured HIF‐1α levels in hypoxic EC cells and further validated the binding of HIF‐1α with LINC01116, analyzing their interaction in EC cells. We then performed experiments in EC109 cells by transfection them with sh‐HIF‐1α/oe‐LINC01116 to verify the effects. Additonally, we analyzed the localization of LINC01116 and its binding with miR‐3612, followed by a combined experiment performed to validate the results. Our findings indicated that LINC01116 was highly expressed in EC and further elevated in hypoxic EC cells. LINC01116 was expressed at a high level in EC, which was further elevated in EC cells under hypoxic conditions. Knockdown of LINC01116 triggered EC cell apoptosis, thus suppressing radioresistance. Further investigation revealed that HIF‐1α transcriptionally activated LINC01116 expression under hypoxia, and silencing HIF‐1α lowered EC cell radioresistance by downregulating LINC01116. Under hypoxic conditions, LINC01116 could function as a sponge for miR‐3612 and inhibit its expression. This interaction between LINC01116 and miR‐3612 played a crucial role in mediating radioresistance in EC cells. Briefly, under hypoxic conditions, HIF‐1α facilitates radioresistance of EC cells by transcriptionally activating LINC01116 expression and downregulating miR‐3612.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Hypoxia‐induced factor‐1α promotes radioresistance of esophageal cancer cells by transcriptionally activating LINC01116 and suppressing miR‐3612 under hypoxia

Zhang,

Wang,

et al. 2023

J Biochem & Molecular Tox

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“…Impairing tumorigenic potential is a common function for miR-3612 in different cancers. 8,10,21,22 For example, miR-3612 targeting the NF receptor associated factor 4 led to the inactivation of NF-κB pathway, thereby suppressing esophageal squamous cell carcinoma. 9 Meanwhile, the elevated level of ETS transcription factor ELK3S effected by the sequestration of miR-3612 favors bladder cancer progression.…”

Section: Discussionmentioning

confidence: 99%

MiR-3612 targeting THBS1 suppresses nasopharyngeal carcinoma progression by PI3K/AKT signaling pathway

Zhang

Cui

et al. 2023

Hum Exp Toxicol

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Background MicroRNA-3612 (miR-3612) is considered a tumor suppressor in different cancers. Nonetheless, its function in nasopharyngeal carcinoma (NPC) has yet to be uncovered. Methods NPC cells and tissues were tested by means of reverse transcription quantitative polymerase chain reaction (RT-qPCR) analysis and western blotting to quantify the expressions of miR-3612 and Thrombospondin 1 (THBS1). Cell Counting Kit-8 (CCK-8) and scratch experiments were carried out to evaluate the migration and proliferation of NPC cells. NPC cell adhesion was also assessed. The predicted interaction of miR-3612 with THBS1 was verified by means of a luciferase reporter assay. In vivo experiments were also conducted to examine how miR-3612 overexpression affects in vivo tumorigenicity. Lastly, phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway status was assessed via western blotting. Results MiR-3612 was downregulated in NPC cells and tissues, whereas THBS1 expression showed an opposite trend. The MiR-3612 mimic inhibited the NPC cell proliferation, adhesion, and migration and also inactivated the PI3K/AKT signaling pathway. Furthermore, miR-3612 mimic also hampered NPC tumorigenesis in vivo. MiR-3612 targeted THBS1 and downregulated THBS1 expression. THBS1 offset the miR-3612-overexpression-induced repression of the migration, adhesion, and proliferation of NPC cells via the activation of the PI3K/AKT pathway. Conclusion MiR-3612 retarded NPC cell migration, adhesion, and proliferation by targeting THBS1 and inactivating the PI3K/AKT signaling pathway. This provides a novel therapeutic approach for NPC intervention.

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“…Moreover, circFNDC3B was overexpressed in ESCC cells and tissues, and circFNDC3B facilitated ESCC cell proliferative, migratory and invasive abilities through the miR-490-3p/HMGA2 axis [ 14 ]. Another report displayed that circ_0006948 knockdown lowered the glycoclastic, proliferative, migrating, and invading capacities of ESCC cells via mediation of the miR-3612/LASP1 axis [ 41 ]. In agreement with these researches, an increase of circFNDC3B expression was also detected in ESCC tissues and cells, and circ_0006948 knockdown lowered ESCC cell glycoclastic, proliferative, migrating, and invading capacities.…”

Section: Discussionmentioning

confidence: 99%

Exosomal circRNA FNDC3B promotes the progression of esophageal squamous cell carcinoma by sponging miR-490-5p and regulating thioredoxin reductase 1 expression

2022

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Exosomal circular RNAs (circRNAs) have been reported to play critical roles in esophageal squamous cell carcinoma (ESCC). We aimed to investigate the function of exosomal circRNA FNDC3B (circFNDC3B). The RNA levels and protein levels were examined using RT-qPCR and western blot (WB) assays. Colony formation and EdU assays were used to assess cell proliferative ability. Cell migratory and invasive abilities were detected by wound healing and transwell assays. Cell apoptosis was measured by flow cytometry. Glycolysis was measured using commercial kits. Transmission electron microscopy (TEM) and nanoparticle tracking analysis (NTA) were applied to examine the morphology and size of exosomes. Dual-luciferase reporter, RIP and RNA pull-down assays assessed the interaction of miR-490-5p with circFNDC3B or thioredoxin reductase 1 (TXNRD1). Xenograft tumor model determined the role of exosomal circFNDC3B in vivo . We observed that circFNDC3B was upregulated in ESCC samples and cells, as well as ESCC-derived exosomes. CircFNDC3B could be delivered via exosomes in tumor cells, and the colony formation, proliferation, migration, invasion, glycolysis, and in vivo growth ability of recipient cells were weakened after co-incubation with exosomal circFNDC3B-knockdown donor cells. CircFNDC3B was a miR-490-5p sponge, and miR-490-5p inhibition reversed the role of exosomal circFNDC3B-downregulating in ESCC cells. TXNRD1 was a miR-490-5p target, and TXNRD1 elevation weakened the anti-cancer function of miR-490-5p upregulation in ESCC cells. CircFNDC3B mediated TXNRD1 expression by interacting with miR-490-5p. In conclusion, exosomal circFNDC3B drove ESCC progression via regulating the miR-490-5p/TXNRD1 axis. Abbreviations EC: esophageal cancer; ESCC: esophageal squamous cell carcinoma; circRNA: circular RNA; WB: western blot; TEM: transmission electron microscopy; NTA: nanoparticle tracking analysis; TXNRD1: thioredoxin reductase 1; IHC: immunohistochemistry; RT-qPCR: reverse transcription-polymerase quantitative chain reaction; GLUT1: glucose transport protein type 1; LDHA: lactate dehydrogenase A

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Circular RNA circ_0006948 Promotes Esophageal Squamous Cell Carcinoma Progression by Regulating microRNA-3612/LASP1 Axis

Cited by 11 publications

References 40 publications

Hypoxia‐induced factor‐1α promotes radioresistance of esophageal cancer cells by transcriptionally activating LINC01116 and suppressing miR‐3612 under hypoxia

Hypoxia‐induced factor‐1α promotes radioresistance of esophageal cancer cells by transcriptionally activating LINC01116 and suppressing miR‐3612 under hypoxia

MiR-3612 targeting THBS1 suppresses nasopharyngeal carcinoma progression by PI3K/AKT signaling pathway

Exosomal circRNA FNDC3B promotes the progression of esophageal squamous cell carcinoma by sponging miR-490-5p and regulating thioredoxin reductase 1 expression

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