Knockdown of long non-coding RNA HOTAIR inhibits cisplatin resistance of gastric cancer cells through inhibiting the PI3K/Akt and Wnt/β-catenin signaling pathways by up-regulating miR-34a

Cheng, Chuanyao; Qin, Yaguang; Zhi, Qiongjie; Wang, Jianjun; Qin, Changjiang

doi:10.1016/j.ijbiomac.2017.10.154

Cited by 136 publications

(98 citation statements)

References 36 publications

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“…For instance, lncRNA HOTAIR might function as a ceRNA in later-stage gastric cancer [28]; lncRNA H19 acted as a competing endogenous RNA in cardiac fibrosis [29]; HOTAIR played its function in cardiac hypertrophy as a ceRNA [9]. In terms of this paper, it was discovered that mRNA HOXA9 was upregulated in PE-treated cardiomyocytes and the silence of HOXA9 attenuated the expressions of ANP and BNP and reduced the cell surface area, all of which were treated with PE.…”

Section: Discussionmentioning

confidence: 84%

lncRNA UCA1 Is a Novel Regulator in Cardiomyocyte Hypertrophy through Targeting the miR-184/HOXA9 Axis

Zhou

Feng

et al. 2018

Cardiorenal Med

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Cardiac hypertrophy is closely associated with a series of cardiovascular diseases, including heart failure and sudden death in particular. An in-depth comprehension of the pathogenesis of cardiac hypertrophy will improve the diagnosis and therapy of cardiac hypertrophy. It has been acknowledged that long noncoding RNAs/microRNAs (lncRNAs/miRNAs) are crucial regulators in diverse biological processes, including various cardiovascular diseases, in multiple manners. Nevertheless, the biological roles of lncRNA UCA1 and miR-184 in cardiac hypertrophy are scarcely reported. In this paper, qRT-PCR analysis exhibited that lncRNA UCA1 was highly expressed in mice heart treated with transverse aortic constriction (TAC) and the cardiomyocytes treated with phenylephrine (PE). On the contrary, miR-184 was downregulated under the same conditions. In addition, it was deduced that lncRNA UCA1 was reversely related with miR-184 in PE-triggered hypertrophic cardiomyocytes, confirmed by the Spearman correlation analysis. The knockdown of UCA1 or the overexpression of miR-184 lessened the enlarged surface area of cardiomyocytes and the elevated expressions of fetal genes (ANP and BNP) induced by PE. Later, it was determined that miR-184 was a direct target of UCA1, whereas the mRNA HOXA9 was a target of miR-184. Rescue assays indicated that UCA1 promoted the progression of cardiac hypertrophy through competitively binding with miR-184 to enhance the expression of HOXA9.

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Section: Discussionmentioning

confidence: 84%

lncRNA UCA1 Is a Novel Regulator in Cardiomyocyte Hypertrophy through Targeting the miR-184/HOXA9 Axis

Zhou

Feng

et al. 2018

Cardiorenal Med

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“…In addition, the expression of lncRNA was also associated with chemoresistance in GC. For example, knocking down lncRNA HOTAIR could up‐regulate miRNA‐34a and inhibit PI3K/Akt and Wnt/β‐catenin signaling pathways, thereby enhancing the anti‐cancer effect of cisplatin (Cheng et al, ). All the above reports indicated that lncRNA played an important role in GC.…”

Section: Discussionmentioning

confidence: 99%

LINC01436, regulating miR‐585 and FBXO11, is an oncogenic lncRNA in the progression of gastric cancer

Zhang

Yang

et al. 2020

Cell Biology International

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Accumulating studies have indicated that long non‐coding RNAs (lncRNAs) are crucial modulators in cancer biology. In this work, we investigated the function and related mechanisms of LINC01436 in the progression of gastric cancer (GC). We demonstrated that LINC01436 was significantly up‐regulated in cancerous tissues of GC samples, and its overexpression was correlated with a worse prognosis for the patients. In the GC cell line BGC823 cells, LINC01436 knockdown repressed the proliferation and metastasis of cancer cells; conversely, in GC cell line AGS cells, overexpression of LINC01436 showed the opposite effects. We then demonstrated that miR‐585, a tumor suppressor, could bind to both LINC01436 and the 3′‐UTR of F‐box protein 11 (FBOX11), and LINC01436 was proved to sponge miR‐585 and repress it, and indirectly promoted the expression of FBOX11. Collectively, these results suggested that LINC01436 was an oncogenic lncRNA in GC and promoted proliferation and metastasis of GC cell via regulating miR‐585 and FBOX11.

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“…16 Researchers have found that HOTAIR knockdown in gastric cancer cells could increase miR-34a levels and inhibit drug resistance. 17 Studies have shown that HOTAIR physically interacts with the miR-34a promoter to silence miR-34a, indicating that HOTAIR can function as competing endogenous RNA for miR-34a. 18,19 Our previous study showed that HOTAIR causes significant upregulation during cellular breast carcinogenesis and was significantly decreased by delphinidin treatment.…”

Section: Patientsmentioning

confidence: 99%

“…miR‐34a, as a tumor suppressor, has been shown to play an important role in carcinogenesis and has low expression in breast cancer tissues and cell lines . Researchers have found that HOTAIR knockdown in gastric cancer cells could increase miR‐34a levels and inhibit drug resistance . Studies have shown that HOTAIR physically interacts with the miR‐34a promoter to silence miR‐34a, indicating that HOTAIR can function as competing endogenous RNA for miR‐34a …”

Section: Introductionmentioning

confidence: 99%

Delphinidin suppresses breast carcinogenesis through the HOTAIR/microRNA‐34a axis

et al. 2019

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Delphinidin, one of the main anthocyanidins, has potent anti‐cancer properties. In this study, we investigated the effect of delphinidin on 1‐methyl‐1‐nitrosourea (MNU)‐induced breast carcinogenesis on rats and the mechanism of delphinidin via negative regulation of the HOTAIR/microRNA‐34a axis. We found administration of delphinidin could effectively suppress MNU‐induced mammal breast carcinogenesis. Delphinidin downregulated the level of HOTAIR and upregulated miR‐34a in breast carcinogenesis. Western blot analysis confirmed that delphinidin treatment can significantly decrease the expression of β‐catenin, glycogen synthase kinase‐3β (Gsk3β), c‐Myc, cyclin‐D1, and matrix metalloproteinase‐7(MMP‐7) expression in breast cancer cells, and inhibition of miR‐34a significantly reduced the effect of delphinidin on c‐Myc, cyclin‐D1, and MMP‐7. HOTAIR overexpression also blocked the effect of delphinidin on miR‐34a and the Wnt/β‐catenin signaling pathway in MDA‐MB‐231 cells. RNA immunoprecipitation (RIP) assay and chromatin immunoprecipitation (ChIP) assay results showed that delphinidin upregulated miR‐34a by inhibiting HOTAIR, coupled with enhancement of the zeste homolog 2 (EZH2) and histone H3 Lys27 trimethylation (H3K27me3). This study indicated that delphinidin may potentially suppress breast carcinogenesis and exert its anti‐cancer effect through the HOTAIR/miR‐34a axis. These findings provided new evidence for the use of delphinidin in preventing breast carcinogenesis.

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Knockdown of long non-coding RNA HOTAIR inhibits cisplatin resistance of gastric cancer cells through inhibiting the PI3K/Akt and Wnt/β-catenin signaling pathways by up-regulating miR-34a

Cited by 136 publications

References 36 publications

lncRNA UCA1 Is a Novel Regulator in Cardiomyocyte Hypertrophy through Targeting the miR-184/HOXA9 Axis

lncRNA UCA1 Is a Novel Regulator in Cardiomyocyte Hypertrophy through Targeting the miR-184/HOXA9 Axis

LINC01436, regulating miR‐585 and FBXO11, is an oncogenic lncRNA in the progression of gastric cancer

Delphinidin suppresses breast carcinogenesis through the HOTAIR/microRNA‐34a axis

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