&lt;p&gt;Knockdown of lncRNA HOXA-AS3 Suppresses the Progression of Atherosclerosis via Sponging miR-455-5p&lt;/p&gt;

et al. 2021

Cancer Cell Int

Background Gastric cancer (GC) is among the most common and deadliest cancers globally. Many long non-coding RNAs (lncRNAs) are key regulators of GC pathogenesis. This study aimed to define the role of HOXA-AS3 in this oncogenic context. Methods Levels of HOXA-AS3 expression in GC were quantified via qPCR. The effects of HOXA-AS3 knockdown on GC cells function were evaluated in vitro using colony formation assays, wound healing assays and transwell assays. Subcutaneous xenograft and tail vein injection tumor model systems were generated in nude mice to assess the effects of this lncRNA in vivo. The localization of HOXA-AS3 within cells was confirmed by subcellular fractionation, and predicted microRNA (miRNA) targets of this lncRNA and its ability to modulate downstream NF-κB signaling in GC cells were evaluated via luciferase-reporter assays, immunofluorescent staining, and western blotting. Results GC cells and tissues exhibited significant HOXA-AS3 upregulation (P < 0.05), and the levels of this lncRNA were found to be correlated with tumor size, lymph node status, invasion depth, and Helicobacter pylori infection status. Knocking down HOXA-AS3 disrupted GC cell proliferation, migration, and invasion in vitro and tumor metastasis in vivo. At a mechanistic level, we found that HOXA-AS3 was able to sequester miR-29a-3p, thereby regulating the expression of LTβR and modulating NF-κB signaling in GC. Conclusion HOXA-AS3/miR-29a-3p/LTβR/NF-κB regulatory axis contributes to the progression of GC, thereby offering novel target for the prognosis and treatment of GC.

Section: Resultssupporting

confidence: 85%

“…There is clear evidence that HOXA-AS3 can function as a ceRNA in the context of HCC, glioma, and atherosclerosis [ 9 , 12 , 20 ]. In HCC, this lncRNA controls the miR-29c/BMP1 axis and thereby promotes tumor cell proliferation, EMT, and metastasis via activating MEK/ERK signaling [ 9 ].…”

Section: Discussionmentioning

confidence: 99%

LncRNA HOXA-AS3 promotes gastric cancer progression by regulating miR-29a-3p/LTβR and activating NF-κB signaling

et al. 2021

Cancer Cell Int

“…4a, b). Such cytoplasmic localization is consistent with the ability of HOXA-AS3 to serve as a ceRNA for speci c miRNAs, as has previously been shown to occur in the context of HCC, glioma, and atherosclerosis [9,12,20]. Using the Starbase v3.0 (http://starbase.sysu.edu.cn) platform [21], we identi ed three putative HOXA-AS3 targets in GC (miR-29a-3p, miR-29b-3p and miR-29c-3p).…”

Section: Hoxa-as3 Binds To Mir-29a-3p In Gc Cellssupporting

confidence: 85%

LncRNA HOXA-AS3 promotes gastric cancer progression by regulating miR-29a-3p/LTβR and activating NF-κB signaling

et al. 2021

Preprint

Background: Gastric cancer (GC) is among the most common and deadliest cancers globally. Many long non-coding RNAs (lncRNAs) are key regulators of GC pathogenesis. This study aimed to define the role of HOXA-AS3 in this oncogenic context. Methods: Levels of HOXA-AS3 expression in GC were quantified via qPCR. The effects of HOXA-AS3 knockdown on GC cells function were evaluated in vitro using colony formation assays, wound healing assays and transwell assays. Subcutaneous xenograft and tail vein injection tumor model systems were generated in nude mice to assess the effects of this lncRNA in vivo. The localization of HOXA-AS3 within cells was confirmed by subcellular fractionation, and predicted microRNA (miRNA) targets of this lncRNA and its ability to modulate downstream NF-κB signaling in GC cells were evaluated via luciferase-reporter assays, immunofluorescent staining, and western blotting.Results: GC cells and tissues exhibited significant HOXA-AS3 upregulation (P<0.05), and the levels of this lncRNA were found to be correlated with tumor size, lymph node status, invasion depth, and Helicobacter pylori infection status. Knocking down HOXA-AS3 disrupted GC cell proliferation, migration, and invasion in vitro and tumor metastasis in vivo. At a mechanistic level, we found that HOXA-AS3 was able to sequester miR-29a-3p, thereby regulating the expression of LTβR and modulating NF-κB signaling in GC. Conclusion: HOXA-AS3/miR-29a-3p/LTβR/NF-κB regulatory axis contributes to the progression of GC, thereby offering novel target for the prognosis and treatment of GC.

“…4a). Such cytoplasmic localization is consistent with the ability of HOXA-AS3 to serve as a ceRNA for speci c miRNAs, as has previously been shown to occur in the context of HCC, glioma, and atherosclerosis [12,13,21]. Using the Starbase v3.0…”

Section: Hoxa-as3 Binds To Mir-29a-3p In Gc Cellssupporting

confidence: 78%

“…There is clear evidence that HOXA-AS3 can function as a ceRNA in the context of HCC, glioma, and atherosclerosis [12,13,21]. In HCC, this lncRNA controls the miR-29c/BMP1 axis and thereby promotes tumor cell proliferation, EMT, and metastasis via activating MEK/ERK signaling [9].…”

Section: Discussionmentioning

confidence: 99%

LncRNA HOXA-AS3 Promotes Gastric Cancer Progression by Regulating miR-29a-3p/LTβR and Activating NF-κB Signaling

et al. 2020

Preprint

Background: Gastric cancer (GC) is among the most common and deadliest cancers globally. While many long non-coding RNAs (lncRNAs) are key regulators of GC pathogenesis, the role of HOXA-AS3 in this oncogenic context remains to be defined. Methods: Levels of HOXA-AS3 expression in GC were quantified, after which the functional role of this lncRNA in vitro and in vivo was assessed via HOXA-AS3 knockdown. The localization of HOXA-AS3 within cells was also confirmed, and predicted microRNA (miRNA) targets of this lncRNA and its ability to modulate downstream NF-κB signaling in GC cells were evaluated.Results: GC cells and tissues exhibited significant HOXA-AS3 upregulation (P<0.05), and the levels of this lncRNA were found to be correlated with tumor size, lymph node status, invasion depth, and Helicobacter pylori infection status. Knocking down HOXA-AS3 disrupted GC cell migration, proliferation, and invasion in vitro and tumor metastasis in vivo. At a mechanistic level, we found that HOXA-AS3 was able to sequester miR-29a-3p, thereby regulating the expression of LTβR and modulating NF-κB signaling in GC. Conclusion: HOXA-AS3/miR-29a-3p/LTβR/NF-κB regulatory axis contributes to the progression of GC, thereby offering novel target for the prognosis and treatment of GC.