Knockdown of lncRNA CCAT1 enhances sensitivity of paclitaxel in prostate cancer via regulating miR-24-3p and FSCN1

Li, Xiaohui; Han, Xingtao; Wei, Pengtao; Yang, Jinhui; Sun, Jiantao

doi:10.1080/15384047.2020.1727700

Cited by 51 publications

(57 citation statements)

References 36 publications

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“…Subsequently, the presence of miR-24-3p caused a reduction of luciferase activity in both DU145-TXR and PC3-TXR cells. In addition, miR-24-3p over-expression led to even more FSCN1 expression in the cells [17]. Gao et al [18] displayed that miR-24-3p was actually downregulated in CC cells, but the miR-24-3p overexpression suppressed the proliferation of CC cells.…”

Section: Discussionmentioning

confidence: 99%

“…Previous research revealed that the prospective downstream targets of CCAT1 included miR-24-3p, which may bind to CCAT1 in RNA pull-down, RIP as well as luciferase assays [17].…”

Section: Discussionmentioning

confidence: 99%

“…It was additionally presented that the rs67085638 C > T SNP in lncRNA CCAT1 was linked to an enhanced risk of colon cancer [21]. Another study showed that CCAT1 may affect the chemoresistance of ovary cancer cells to PTX via regulating miR-24-3p and FSCN1 [17]. In this study, we investigated the effect of rs67085638 on the expression of CCAT1/miR-24-3p/FSCN1 and the response of colon cancer to the treatment of PTX.…”

mentioning

confidence: 94%

“…In the last few years, miR-24-3p has been extensively studied as a tumor suppressor in many types of tumors, including nasopharyngeal carcinoma, liver cancer, as well as lung cancer, indicating that miR-24-3p contributes in the process of tumor growth suppression as well as enhancing the apoptosis of tumor cells [15,16]. It was actually presented that the expression of miR-24-3p was negatively moderated via CCAT1, while the depletion of miR-24-3p eliminated the suppressive impact of knockdown of CCAT1 on PTX resistance, suggesting that CCAT1 managed PTX resistance through sponging the expression of miR-24-3p [17]. Li et al have shown that miR-24 could reduce the migration, proliferation, invasion as well as growth of tumor cells through targeting the FSCN1 expression in nasopharyngeal cancer [17].…”

mentioning

confidence: 98%

“…It was actually presented that the expression of miR-24-3p was negatively moderated via CCAT1, while the depletion of miR-24-3p eliminated the suppressive impact of knockdown of CCAT1 on PTX resistance, suggesting that CCAT1 managed PTX resistance through sponging the expression of miR-24-3p [17]. Li et al have shown that miR-24 could reduce the migration, proliferation, invasion as well as growth of tumor cells through targeting the FSCN1 expression in nasopharyngeal cancer [17].…”

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confidence: 99%

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Effect of rs67085638 in long non-coding RNA (CCAT1) on colon cancer chemoresistance to paclitaxel through modulating the microRNA-24-3p and FSCN1 signaling

Zhang

Wang

2020

Preprint

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BackgroundIt has been reported that rs67085638 in lncRNA-CCAT1 was associated with the risk of tumorigenesis. Also, CCAT1 could affect chemoresistance of cancer cells to PTX via regulating miR-24-3p and FSCN1 expression. In this study, we aimed to investigate the effect of rs67085638 on the expression of CCAT1/miR-24-3p/FSCN1 and the response of colon cancer to the treatment of PTX.Method48 colon cancer patients were recruited and grouped by their genotypes of rs67085638 polymorphism as a CC group (N=28) and a CT group (N=20). Colon cancer cells were collected from the patients and cancer cell xenografts were transplanted into mice. PCR analysis, IHC assay and Western blot were performed to observe the expression of lncRNA-CCAT1, miR-24-3p and FSCN1 in vivo and in vitro, and the relationships among the expression of lncRNA-CCAT1, miR-24-3p and FSCN1 were validated by computational analysis and luciferase assay. TUNEL assay and flow cytometry were conducted to observe tumor cell apoptosis and survival.ResultLncRNA-CCAT1 and FSCN1 mRNA/protein were over-expressed while miR-24-3p was down-regulated in the CT-genotyped patients and cells compared with those in the CC-genotyped patients and cells. The survival of colon cancer cells was decreased while the apoptosis of colon cancer cells was increased by PTX treatment in a dose-dependent manner. However, the survival rate of CT-genotyped cells was higher while the apoptosis rate of CT-genotyped cells was lower than that of the CC-genotyped cells, and the difference was partly eliminated by the knockdown of lncRNA-CCAT1. MiR-24-3p was validated to target lncRNA-CCAT1 and FSCN1 mRNA, and the over-expression of CCAT1 could reduce the expression of miR-24-3p while elevating the expression of FSCN1. The growth of CT-genotyped tumors in mice was more suppressed in compared with the growth of CC-genotyped tumors, while the knockdown of lncRNA-CCAT1 partly reversed the effect of the CT genotype. Furthermore, compared with the rs67085638-CC mice, the lncRNA-CCAT1 and FSCN1 mRNA/protein levels in the rs67085638-CT+NC shRNA mice were increased while their miR-24-3p level was decreased, and the knockdown of lncRNA-CCAT1 partly reversed the dysregulation of these genes.ConclusionThe findings of this study demonstrated that the presence of the minor allele of rs67085638 increased the expression of CCAT1 and accordingly enhanced the resistance to PTX. Downregulation of CCAT1 partially, but significantly, re-stored the sensitivity to PTX of colon cancer cells.

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Section: Discussionmentioning

confidence: 99%

“…Previous research revealed that the prospective downstream targets of CCAT1 included miR-24-3p, which may bind to CCAT1 in RNA pull-down, RIP as well as luciferase assays [17].…”

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 94%

mentioning

confidence: 98%

mentioning

confidence: 99%

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Effect of rs67085638 in long non-coding RNA (CCAT1) on colon cancer chemoresistance to paclitaxel through modulating the microRNA-24-3p and FSCN1 signaling

Zhang

Wang

2020

Preprint

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Silencing LINC00491 inhibits prostate cancer development through the miR‐384/TRIM44 axis

Zhou

Tang

et al. 2023

J Biochem & Molecular Tox

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Accumulating evidence has demonstrated the key role of long noncoding (lnc) RNAs in tumorigenesis. Prostate cancer (PCa) is a cancer with high mortality that requires further exploration of the underlying molecular mechanisms. In the present study, we aimed to discover novel potential biomarkers for diagnosing PCa and targeting treatment. Overexpression of the lncRNA, LINC00491, was verified in PCa tumor tissues and cell lines using the realtime polymerase chain reaction. Cell proliferation and invasion were then analyzed via the Cell Counting Kit-8, colony formation, and transwell assays in vitro, and tumor growth in vivo. The interaction of miR-384 with LINC00491, as well as TRIM44, was investigated via bioinformatics analyses, subcellular fractionation, luciferase reporter gene assays, radioimmunoprecipitation, pulldown, and western blot analyses. LINC00491 was overexpressed in PCa tissues and cell lines. LINC00491 knockdown resulted in impaired cell proliferation and invasion in vitro and decreased tumor growth in vivo. Moreover, LINC00491 acted as a sponge for miR-384 and its downstream target, TRIM44. Additionally, miR-384 expression was downregulated in PCa tissues and cell lines, and its expression was negatively correlated with LINC00491. A miR-384 inhibitor restored the inhibitory effects of LINC00491 silencing on PCa cell proliferation and invasion. LINC00491 is a tumor promoter in PCa via enhancing TRIM44 expression by sponging miR-384 to facilitate the development of PCa.LINC00491 plays a significant role in PCa and could serve as both a biomarker for early diagnosis and a novel treatment target.

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LncRNA CCAT1 downregulation increases the radiosensitivity of non‐small cell lung cancer cells

Zhao

2021

The Kaohsiung J of Med Scie

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This study aims to investigate if the radiosensitivity of non-small cell lung cancer (NSCLC) cells can be regulated by long noncoding RNA (lncRNA) colon cancer associated transcript1 (CCAT1). CCAT1 was detected by quantitative reverse transcriptionpolymerase chain reaction (qRT-PCR) in NSCLC cells (A549, H1299, SK-MES1, H460, and H647) and human bronchial epithelial cells (16HBE). H460 and A549 cells were then selected for the determination of CCAT1 expression after exposure to radiation (0, 2, 4, 6 Gy) at different time points (0, 6, 12, 24 h). Colony forming assay was performed to evaluate the effects of CCAT1 siRNA or pcDNA3.1-CCAT1 vector on the radiosensitivity of H460 and A549 cells. Then, flow cytometry, western blotting and qRT-PCR were also conducted. CCAT1 was increased in NSCLC cells when compared with 16HBE cells, which was declined in a time-and dosage-dependent manner after exposure to radiation. The H460 and A549 cell colonies were decreased and the γ-H2AX expression was elevated with the increase of radiation dosage, which was more obvious in those transfected with CCAT1 siRNA. CCAT1 downregulation arrested NSCLC cells at G2/M phase. Moreover, the enhanced apoptosis of radiotherapy-treated NSCLC cells with reductions of p-p38/p38, p-ERK/ ERK, and p-JNK/JNK was promoted by siCCAT1, but it was reversed by pcDNA3.1-CCAT1 vector. Inhibiting CCAT1 regulated cell cycle, DNA damage and apoptosis of NSCLC cells, and affected MAPK pathway, eventually improving the radiosensitivity of NSCLC.

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Knockdown of lncRNA CCAT1 enhances sensitivity of paclitaxel in prostate cancer via regulating miR-24-3p and FSCN1

Cited by 51 publications

References 36 publications

Effect of rs67085638 in long non-coding RNA (CCAT1) on colon cancer chemoresistance to paclitaxel through modulating the microRNA-24-3p and FSCN1 signaling

Effect of rs67085638 in long non-coding RNA (CCAT1) on colon cancer chemoresistance to paclitaxel through modulating the microRNA-24-3p and FSCN1 signaling

Silencing LINC00491 inhibits prostate cancer development through the miR‐384/TRIM44 axis

LncRNA CCAT1 downregulation increases the radiosensitivity of non‐small cell lung cancer cells

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