lncRNA LUNAR1 accelerates colorectal cancer progression by targeting the miR‑495‑3p/MYCBP axis

Qian, Jin-yuan; Garg, Alok; Li, Fuqiang; Shen, Qianyun; Ke, Xiaoyan

doi:10.3892/ijo.2020.5128

Cited by 17 publications

(18 citation statements)

References 37 publications

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“…Importantly, the current data indicated that NORAD could function as competitive endogenous RNA to regulate HIF-1α expression by directly sponging miR-495-3p. Of note, miR-495 can act as a suppressor in CRC cell proliferation, migration, and invasion [ 20 , 37 ]. More interestingly, previous evidence supported miR-495 as a chemoradiotherapy-sensitive gene in CRC patients [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

Induction of lncRNA NORAD accounts for hypoxia-induced chemoresistance and vasculogenic mimicry in colorectal cancer by sponging the miR-495-3p/ hypoxia-inducible factor-1α (HIF-1α)

Zhang

et al. 2021

Bioengineered

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Hypoxic microenvironment represents the hallmark of solid tumors including colorectal cancer (CRC) and facilitates angiogenesis and chemoresistance, leading to poor prognosis. lncRNA NORAD acts as an oncogenic gene to orchestrate cancer progression by regulating cell proliferation and migration. Notably, an emerging study corroborates the elevation of NORAD during hypoxic conditions in pancreatic cancer. Nevertheless, its biological role in hypoxia-evoked CRC remains unclear. Herein, enhanced expression of NORAD and hypoxia-inducible factor-1α (HIF-1α) was validated in CRC tissues. Furthermore, there was a positive association between NORAD and HIF-1α in CRC tissues. CRC cells exposed to hypoxia exhibited a stronger ability to form vasculogenic mimicry (VM) and resistance to 5-fluorouracil (5-FU), concomitant with higher expression of NORAD. NORAD knockdown restrained hypoxia-induced VM formation and VM marker VE-cadherin expression. Moreover, knockdown of NORAD counteracted CRC cell resistance to 5-FU by decreasing cell viability and increasing cell apoptosis. Additionally, NORAD loss reduced hypoxia-induced HIF-1α expression and subsequent epithelial-mesenchymal transition (EMT) by increasing E-cadherin and inhibiting N-cadherin expression. Intriguingly, HIF-1α overexpression reversed NORAD downregulation-mediated inhibition of VM formation and 5-FU resistance. There was a low expression of miR-495-3p in CRC tissues. Furthermore, NORAD could act as a competitive endogenous RNA of miR-495-3p to regulate HIF-1α. Importantly, inhibition of miR-495-3p muted the efficacy of NORAD loss in hypoxia-induced EMT, VM, and chemoresistance. Thus, the current data highlight that NORAD knockdown may antagonize hypoxia-triggered CRC malignancy by suppressing VM formation and chemoresistance by sponging miR-495-3p/HIF-1α to regulate EMT, supporting a promising therapeutic target for refractory hypoxia in CRC.

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Section: Discussionmentioning

confidence: 99%

Induction of lncRNA NORAD accounts for hypoxia-induced chemoresistance and vasculogenic mimicry in colorectal cancer by sponging the miR-495-3p/ hypoxia-inducible factor-1α (HIF-1α)

Zhang

et al. 2021

Bioengineered

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“…Many analyses have highlighted the essential regulatory roles of lncRNAs in oncogenic contexts. For example, CASC7 is a lncRNA that suppresses miR-10a and thereby upregulates PTEN to suppress the proliferation of neuroblastoma cells, 15 while LUNAR1 is a lncRNA that can modulate the miR4953p/MYCBP axis to promote colorectal cancer progression, 16 and TUG1 can sequester miR-1294 to upregulate PLK1 and thereby drive esophageal cancer development. 17 MAGI1‐IT1 has been found to play an oncogenic role in non-small-cell lung cancer wherein it serves as a ceRNA to upregulate AKT1, 8 and in epithelial ovarian cancer wherein it can control the miR-200a/ZEB axis to promote tumor metastasis.…”

Section: Discussionmentioning

confidence: 99%

The Long Noncoding RNA MAGI1-IT1 Regulates the miR-302d-3p/IGF1 Axis to Control Gastric Cancer Cell Proliferation

Wang¹,

Gu²,

Zhuang³

et al. 2021

CMAR

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Background: MAGI1-IT1 is a long non-coding RNA (lncRNA) previously reported to regulate several cancer types, but its functional role in gastric cancer (GC) remains to be defined. This study therefore explored the mechanistic role played by MAGI1-IT1 in the regulation of GC cell proliferation. Methods: 120 pairs of GC patient tumor, paracancerous tissues, human GES-1 control cells and human AGS, MKN-74, MKN-45, and MGC-803 GC cell lines were used to detected MAGI1-IT1, miR-302d-3p, and IGF1 expression by a qPCR approach. An shRNA approach was used to knock down MGI1-IT1 in order to examine the effect of such treatment on GC cell proliferation, and rescue experiments were subsequently conducted. In addition, the functional role of MAGI1-IT1 in GC in vivo was evaluated with a xenograft model system. P < 0.05 was the significance threshold. Results: Elevated MAGI1-IT1 expression was detected in GC cell lines and tissues, and was linked to poorer patient overall survival. Knocking down this lncRNA disrupted GC cell proliferation in vitro and in vivo, and miR-302d-3p was identified as a MAGI1-IT1 target. Notably, miR-302d-3p inhibition partially reversed the impact of MAGI1-IT1 knockdown on GC cell proliferation. IGF1 was subsequently identified as a miR-302d-3p target gene that was upregulated by MAGI1-IT1 through miR-302d-3p. Conclusion: Overall, these results indicated that MAGI1-IT1 controlled GC cell proliferation by modulating the miR-302d-3p/IGF1 axis, suggesting that this may be a viable treatment target in those with GC.

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“…According to previous studies, miR-495-3p exerted a tumor suppressive effect in several cancer types. For instance, miR-495-3p expression was found to be downregulated in colorectal cancer ( 35 ). Moreover, miR-495-3p restrained the proliferation, invasion and migration of osteosarcoma cells by directly targeting complement C1q/TNF-related protein 3 ( 36 ).…”

Section: Discussionmentioning

confidence: 99%

Silencing circ‑BIRC6 inhibits the proliferation, invasion, migration and epithelial‑mesenchymal transition of bladder cancer cells by targeting the miR‑495‑3p/XBP1 signaling axis

et al. 2021

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Circular RNAs (circRNAs) regulate gene expression by acting as a ‘sponge’ for microRNAs (miRs) and play crucial roles in tumorigenesis, including in bladder cancer (BC). circRNA-baculoviral IAP repeat-containing 6 (circ-BIRC6) has been reported to participate in the pathogenesis of several cancer types. The present study aimed to elucidate the roles and potential mechanisms of circ-BIRC6 in the progression of BC. circ-BIRC6 expression levels in BC cell lines were determined using reverse transcription-quantitative PCR. Following circ-BIRC6 knockdown, cell proliferation, invasion and migration were detected using Cell Counting Kit-8, colony formation, Transwell and wound healing assays, respectively. Western blotting was also conducted to evaluate the expression levels of X-box binding protein 1 (XBP1) and epithelial-mesenchymal transition (EMT)-associated proteins. In addition, rescue experiments were performed using by transfecting a miR-495-3p inhibitor into T24 cells following circ-BIRC6 knockdown. The interactions between circ-BIRC6, miR-495-3p and XBP1 was verified using dual luciferase reporter assays. Moreover, T24 cells with circ-BIRC6 knockdown and miR-495-3p inhibitor transfection were used for the tumor-bearing experiment. Tumor growth was observed and Ki-67 expression was determined using immunohistochemistry. The results demonstrated that circ-BIRC6 expression was upregulated in BC cell lines. Moreover, circ-BIRC6 knockdown notably attenuated the proliferation, invasion, migration and EMT of BC cells, which was blocked by the miR-495-3p inhibitor. It was also identified that circ-BIRC6 sponged miR-495-3p to regulate XBP1 expression. In addition, results from the xenograft experiments indicated that the knockdown of circ-BIRC6 and miR-495-3p expression significantly inhibited tumor growth. It was also found that the expression levels of XBP1, Ki-67 and EMT-associated proteins in tumor tissues of the co-transfection group were markedly restored compared with the circ-BIRC6 knockdown group. In conclusion, these findings demonstrated that circ-BIRC6 knockdown suppressed BC tumorigenesis and progression via regulation of the miR-495-3p/XBP1 signaling axis, offering a promising therapeutic target for the treatment of BC.

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lncRNA LUNAR1 accelerates colorectal cancer progression by targeting the miR‑495‑3p/MYCBP axis

Cited by 17 publications

References 37 publications

Induction of lncRNA NORAD accounts for hypoxia-induced chemoresistance and vasculogenic mimicry in colorectal cancer by sponging the miR-495-3p/ hypoxia-inducible factor-1α (HIF-1α)

Induction of lncRNA NORAD accounts for hypoxia-induced chemoresistance and vasculogenic mimicry in colorectal cancer by sponging the miR-495-3p/ hypoxia-inducible factor-1α (HIF-1α)

The Long Noncoding RNA MAGI1-IT1 Regulates the miR-302d-3p/IGF1 Axis to Control Gastric Cancer Cell Proliferation

Silencing circ‑BIRC6 inhibits the proliferation, invasion, migration and epithelial‑mesenchymal transition of bladder cancer cells by targeting the miR‑495‑3p/XBP1 signaling axis

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