RETRACTED ARTICLE: Long non-coding RNA 00960 promoted the aggressiveness of lung adenocarcinoma via the miR-124a/SphK1 axis

Ge, Zhipeng; Li, Haibo; Ji, Tao; Liu, Qiaoling; Zhang, Lulu; Zhu, Pengchong; Li, Liang; Zhu, Luyi

doi:10.1080/21655979.2021.1996507

Cited by 11 publications

(10 citation statements)

References 50 publications

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“…12 In lung adenocarcinoma (LADC), LINC00960 mediated the miR-124a/ sphingosine kinase 1 axis to induce LADC development by promoting cell proliferation, migration, and invasion. 22 We obtained similar outcomes, that is, LINC00960 silencing impeded PC cell proliferation.…”

Section: Discussionsupporting

confidence: 62%

“…Another study showed that LINC00960 accelerated cell growth and metastasis in PDAC by inhibiting the miR‐146a‐5p / IRAK1 axis 12 . In lung adenocarcinoma (LADC), LINC00960 mediated the miR‐124a /sphingosine kinase 1 axis to induce LADC development by promoting cell proliferation, migration, and invasion 22 . We obtained similar outcomes, that is, LINC00960 silencing impeded PC cell proliferation.…”

Section: Discussionsupporting

confidence: 55%

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LINC00960 regulates cell proliferation and glycolysis in pancreatic cancer through the miR‐326‐3p/TUFT1/AKT–mTOR axis

Zhou

Lei

Wang

et al. 2022

The Kaohsiung J of Med Scie

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Pancreatic cancer (PC) is a common malignant cancer characterized by high mortality and poor prognosis. LINC00690 was involved in the occurrence and progression of PC, but the underlying mechanisms require further investigation. The goal of this study was to figure out how LINC00960 mediates glycolysis in PC. LINC00960, miR-326-3p, and Tuftelin 1 (TUFT1) expression levels were detected in PC cell lines.LINC00960 and TUFT1 expression levels were increased in PC cells when compared with normal pancreatic cells, whereas miR-326-3p expression levels were decreased.The expression levels of LINC00690 affected glycolysis in PC, and inhibition of LINC00960 inhibited tumor growth in vivo. LINC00690 targeted and suppressed the expression of miR-326-3p. MiR-326-3p bound to TUFT1, and miR-326-3p inhibited AKT-mTOR pathway activation via TUFT1. In conclusion, the depletion of LINC00960 repressed cell proliferation and glycolysis in PC by mediating the miR-326-3p/TUFT1/AKT-mTOR axis. Thus, we present a novel mechanism underlying the progression of PC that suggests LINC00960 is a potential therapeutic target for this cancer.

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Section: Discussionsupporting

confidence: 62%

Section: Discussionsupporting

confidence: 55%

LINC00960 regulates cell proliferation and glycolysis in pancreatic cancer through the miR‐326‐3p/TUFT1/AKT–mTOR axis

Zhou

Lei

Wang

et al. 2022

The Kaohsiung J of Med Scie

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“…LINC00960 bears closer potential binding sites with miR-183-5p than Nrdp1 ( Figure 3 A). A few miRNAs have been reported to be targeted by LINC00960 [ 18 – 21 ] , but LINC00960 bears the highest score to complement miR-183-5p ( ). Several lncRNAs or circRNAs have also been shown to target miR-183-5p [ 22 – 28 ] , but LINC00960 ranks at the top among all these noncoding RNAs ( ).…”

Section: Resultsmentioning

confidence: 99%

“…lncRNA PVT1 in exosomes promotes osteosarcoma growth and metastasis by sponging miR-183-5p [24] . LINC00960 was found to play an active role in promoting the malignant behaviors of bladder cancer cells [59] , pancreatic ductal adenocarcinoma [19] , lung adenocarcinoma [18] , and osteosarcoma [60] . Interestingly, LINC00960 was also shown to promote lung adenocarcinoma by sponging miR-124a, the latter of which suppresses the expression of SphK1 [18] and regulates cell viability, migration and invasion in pancreatic ductal adenocarcinoma by modulating miR-146a-5p, which targets interleukin 1 receptor-associated kinase 1 [19] .…”

Section: Discussionmentioning

confidence: 99%

lncRNA LINC00960 promotes apoptosis by sponging ubiquitin ligase Nrdp1-targeting miR-183-5p

Yang¹,

Jiang²,

Фан³

et al. 2023

ABBS

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The ubiquitin ligase Nrdp1/RNF41 promotes the ubiquitin-dependent degradation of multiple important substrates, including BRUCE/BIRC6, a giant ubiquitin-conjugating enzyme inhibiting both apoptosis and autophagy. miR-183-5p is associated with various malignancies potentially by targeting dozens of genes. Here, we show that the lncRNA LINC00960 binds to the Nrdp1-targeting miR-183-5p and promotes apoptosis. Compared to other known miR-183-5p targets, Nrdp1 mRNA is among the few with top scores to complement miR-183-5p. miR-183-5p binds to the 3′UTR of Nrdp1 mRNA and downregulates Nrdp1 at both the mRNA and protein levels. The miR-183-5p mimics inhibit DNA damage-induced apoptosis probably by upregulating BRUCE level, whereas the miR-183-5p inhibitor suppresses the effects of miR-183-5p. LINC00960 is the noncoding RNA with the highest score to complement miR-183-5p. LINC00960 overexpression reduces, but its knockdown increases, the level of miR-183-5p, whereas LINC00960 overexpression increases, but its knockdown decreases, the level of Nrdp1 and apoptosis. Importantly, the expression of LINC00960, which is associated with multiple types of tumors, positively correlates with that of Nrdp1 in several tumors but inversely correlates with that of miR-183-5p in multiple human tumor cell lines, as analysed by quantitative PCR. Thus, miR-183-5p downregulates Nrdp1 expression and inhibits apoptosis, whereas LINC00960 upregulates Nrdp1 and promotes apoptosis by inhibiting miR-183-5p. These results may provide new ideas for the prevention, diagnosis and treatment of apoptosis-related diseases, such as tumors and neurodegenerative diseases.

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“…The complexes were then incubated with Streptavidin agarose beads (Invitrogen) for 1 h at 37°C. The beads were washed, and RNA level were analyzed by qRT-PCR [ 29 ].…”

Section: Methodsmentioning

confidence: 99%

MicroRNA-122-3p plays as the target of long non-coding RNA LINC00665 in repressing the progress of arthritis

Wang

Tian

et al. 2022

Bioengineered

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MicroRNAs (miRNAs) play important roles in many diseases, including rheumatoid arthritis (RA). However, the mechanisms underlying the effects of miR-122-3p-3p on RA are not distinct and require further investigation. Patients with RA and healthy controls were recruited to analyze the miR-122-3p levels. The MH7A cells were stimulated with interleukin (IL)-1β to mimic the local inflammation of RA. Cell Counting Kit-8 (CCK-8) and flow cytometry were performed to measure the viability and apoptosis of MH7A cells. Diana tools and TargetScan were used to predict the target relationships. Luciferase reporter assay was used to validate the target relationship. miR-122-3p is downregulated in RA patients and IL-1β-stimulated MH7A cells. miR-122-3p suppresses MH7A cell viability and promotes MH7A cell apoptosis. miR-122-3p targets LINC00665. LINC00665 eliminates the inhibitory effect of miR-122-3p on IL-1β-stimulated MH7A cells. Eukaryotic translation initiation factor 2 alpha kinase 1 (EIF2AK1) targets miR-122-3p. In addition, EIF2AK1 is highly expressed in patients with RA. In addition, EIF2AK1 activates the mTOR signaling pathway. miR-122-3p represses RA progression by reducing cell viability and increasing synoviocyte apoptosis.

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RETRACTED ARTICLE: Long non-coding RNA 00960 promoted the aggressiveness of lung adenocarcinoma via the miR-124a/SphK1 axis

Cited by 11 publications

References 50 publications

LINC00960 regulates cell proliferation and glycolysis in pancreatic cancer through the miR‐326‐3p/TUFT1/AKT–mTOR axis

LINC00960 regulates cell proliferation and glycolysis in pancreatic cancer through the miR‐326‐3p/TUFT1/AKT–mTOR axis

lncRNA LINC00960 promotes apoptosis by sponging ubiquitin ligase Nrdp1-targeting miR-183-5p

MicroRNA-122-3p plays as the target of long non-coding RNA LINC00665 in repressing the progress of arthritis

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