The action mechanism of lncRNA-HOTAIR on the drug resistance of non-small cell lung cancer by regulating Wnt signaling pathway

Guo, Feng; Cao, Zhili; H, Guo; Li, Shanqing

doi:10.3892/etm.2018.6052

Cited by 42 publications

(41 citation statements)

References 20 publications

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“…Previous studies have revealed that the expression of multidrug resistance genes is closely associated with lncRNAs in tumors (22,27); silencing of lncRNA metastasis-associated lung adenocarcinoma transcript decreased MDR1, MRP5 and prolow-density lipoprotein receptor-related protein 1 (LRP1) expression levels and reversed temozolomide resistance in glioblastoma cells (28). Additionally, downregulation of lncRNA X-inactive specific transcript inhibited GSTπ expression, promoted apoptosis and increased the sensitivity of colorectal cancer cells to doxorubicin (29).…”

Section: Discussionmentioning

confidence: 99%

Knockdown of long non‑coding RNA LINC00152 increases cisplatin sensitivity in ovarian cancer cells

Zou

2019

Exp Ther Med

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Drug resistance severely limits the effectiveness of chemotherapeutic treatment in ovarian cancer. The present study aimed to investigate the role of long non-coding RNA LINC00152 (LINC00152) in the cisplatin resistance of ovarian cancer. The expression level of LINC00152 was significantly increased in the ovarian cancer CoC1 and CoC1/DDP cell lines compared with the normal ovarian IOSE-80 cell line. To further investigate the function of LINC00152, small interfering RNAs (siRNAs) targeting LINC00152 were transfected into COC1 and COC1/DDP cells, which were subsequently treated with varying concentrations of cisplatin. The results revealed that LINC00152 silencing increased the apoptotic rates and enhanced the chemosensitivity of CoC1 and CoC1/DDP cells to cisplatin. Furthermore, downregulation of LINC00152 significantly decreased Bcl-2, and increased Bax and cleaved caspase-3 expression levels. Additionally, LINC00152 silencing decreased the expression of multidrug resistance-associated gene 1 (MDR1), multidrug resistance-associated protein 1 (MRP1) and glutathione S-transferase π (GSTπ). Collectively, the data demonstrated that LINC00152 knockdown increased the chemosensitivity of epithelial ovarian cancer cells to cisplatin by increasing apoptosis and decreasing the expression levels of MDR1, MRP1 and GSTπ. Materials and methods Cell culture. The human normal ovarian cells line IOSE-80, ovarian adenocarcinoma cell line COC1 and its cisplatin-resistant variant COC1/DDP were obtained from the China Center for Type Culture Collection. The cells were cultured in RPMI-1640 supplemented with 10% fetal bovine serum (Gibco; Thermo Fisher Scientific, Inc.,) at 37˚C in a

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Section: Discussionmentioning

confidence: 99%

Knockdown of long non‑coding RNA LINC00152 increases cisplatin sensitivity in ovarian cancer cells

Zou

2019

Exp Ther Med

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“…HOTAIR is a highly studied lncRNA. Previous studies demonstrated that it serves a role in the development and progression of various types of solid tumor, including renal cell carcinoma, colorectal cancer, breast cancer, gastric cancer, non-small cell lung cancer, cervical cancer and ovarian epithelial carcinoma (35)(36)(37)(38)(39)(40)(41)(42)(43)(44)(45). In addition, Ren et al (46) demonstrated that HOTAIR can control the cell cycle by acting as a competing endogenous 'sponge' to downregulate miR-1 and upregulate cyclin D1 in ESCC.…”

Section: Identification Of Demirnasmentioning

confidence: 99%

Cancer‑related long noncoding RNAs show aberrant expression profiles and competing endogenous RNA potential in esophageal adenocarcinoma

Chen

Cang

2019

Oncol Lett

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Long non-coding RNAs (lncRNAs) govern gene expression by competitively binding to microRNA response elements (MREs). Although they were initially considered as transcriptional noise, lncRNAs have attracted increased attention in oncology. Dysregulation of lncRNAs occurs in various types of human tumor, including esophageal adenocarcinoma (EAC). However, the functions of these cancer-associated lncRNAs and of their related competitive endogenous RNA (ceRNA) network in EAC remains unknown. To determine the relevant potential mechanisms, the present study analyzed the transcriptome sequencing data and clinical information of 79 patients with EAC, including 79 tumor samples and 11 normal samples, which were obtained from The Cancer Genome Atlas esophageal cancer project. The edgeR v3.25.0 software was used for differential gene expression analysis. The results exhibited 561 cancer-associated lncRNAs with a >2.0-fold change and a false discovery rate-adjusted P<0.01. Among these lncRNAs, 26 were significantly associated with patient overall survival. According to data from bioinformatics databases and differentially expressed RNAs, an lncRNA-regulated ceRNA network for EAC was constructed. The results demonstrated that the aberrantly expressed lncRNA-associated ceRNA network included 37 EAC cancer-associated lncRNAs, five miRNAs and 13 mRNAs. In conclusion, the present study identified novel lncRNAs as candidate prognostic biomarkers and revealed a potential regulatory network of gene expression in EAC.

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“…The Wnt signaling pathway plays important roles in the carcinogenesis of several types of cancers, especially colon cancer, . HOTAIR was shown to activate Wnt pathway through inhibition of WIF‐1 expression, and could participate in the drug resistance . Furthermore, STAT3 (signaling transducer and activator of transcription 3) has been proved to regulate the activity of HOTAIR, and influence the biological functions of cervical cancer .…”

Section: Introductionmentioning

confidence: 99%

“…23 HOTAIR was shown to activate Wnt pathway through inhibition of WIF-1 expression, 17 and could participate in the drug resistance. 24 Furthermore, STAT3 (signaling transducer and activator of transcription 3) has been proved to regulate the activity of HOTAIR, and influence the biological functions of cervical cancer. 25 In addition, STAT3 could also promote epithelial-mesenchymal transition (EMT) in colon cancer, thus contributing to the cancer metastasis.…”

mentioning

confidence: 99%

Effects of propofol on colon cancer metastasis through STAT3/HOTAIR axis by activating WIF‐1 and suppressing Wnt pathway

Zhang

Zhou

et al. 2020

Cancer Medicine

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Background In the present study, we aim to investigate the potential role of propofol in the tumor progression of colon cancer. Methods Human colon cancer cell lines were cultured and exposed with 8 μg/mL propofol. RNA interference was performed to silence the expression of HOTAIR or STAT3 to explore their biological functions in colon cancer. Cell apoptosis and invasion were assessed using flow cytometry and transwell assays, respectively. Quantitative real‐time PCR, western blot, and immunohistochemistry were subjected to measure the expression patterns of HOTAIR, STAT3, Wnt signaling factors, and epithelial‐mesenchymal transition‐related markers, respectively. Besides, nude mice were transplanted with colon cancer cells for further exploration. Tumor formation, volume, and weight were evaluated to validate the in vitro findings. Results Propofol treatment promoted cell apoptosis and inhibited cell invasion in colon cancer cells, while the effects were reversed by HOTAIR overexpression. Additionally, STAT3 positively regulated HOTAIR expression, which was also negatively modulated by propofol. Moreover, STAT3 and HOTAIR were shown to independently regulate colon cancer cell apoptosis and invasion. Furthermore, HOTAIR could stimulate Wnt signaling pathway via inhibiting WIF‐1 expression and upregulating β‐catenin expression, which was also demonstrated by in vivo study. Conclusion Taken together, the current study demonstrated that propofol exerts the inhibition on cell invasion and promotion on cell apoptosis through regulating STAT3/HOTAIR by activating WIF‐1 and suppressing Wnt pathway, indicating that propofol might serve as a therapeutic role for colon cancer patients in the future.

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The action mechanism of lncRNA-HOTAIR on the drug resistance of non-small cell lung cancer by regulating Wnt signaling pathway

Cited by 42 publications

References 20 publications

Knockdown of long non‑coding RNA LINC00152 increases cisplatin sensitivity in ovarian cancer cells

Knockdown of long non‑coding RNA LINC00152 increases cisplatin sensitivity in ovarian cancer cells

Cancer‑related long noncoding RNAs show aberrant expression profiles and competing endogenous RNA potential in esophageal adenocarcinoma

Effects of propofol on colon cancer metastasis through STAT3/HOTAIR axis by activating WIF‐1 and suppressing Wnt pathway

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