LncRNA BCAR4 promotes colon cancer progression via activating Wnt/β-catenin signaling

Ouyang, Shurui; Zheng, Xinbin; Zhou, Xin; Chen, Zhengquan; Yang, Xuefeng; Xie, Ming

doi:10.18632/oncotarget.21590

Cited by 47 publications

(40 citation statements)

References 39 publications

(39 reference statements)

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“…Previous studies have suggested that lncRNA dysregulation in NSCLC is associated with lymph node metastasis, advanced stage, metastasis development, and poor patient prognosis. Anti‐tumor drug resistance in various carcinomas, including colon, bladder, ovarian, and gastric cancers, and NSCLC, is associated with lncRNAs. Although advances have been achieved in diagnosis and treatment, NSCLC is still one of the most common malignancies, with five‐year survival rates < 15% .…”

Section: Resultsmentioning

confidence: 99%

Role of long non‐coding RNA in drug resistance in non‐small cell lung cancer

Wang

et al. 2018

Thoracic Cancer

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Lung cancer is the leading cause of cancer‐associated death, and non‐small cell lung cancer (NSCLC) accounts for 85% of all lung cancer cases. Many drugs have been used to treat NSCLC in order to improve patient prognosis. Platinum‐based chemotherapy is the first‐line treatment for locally advanced or metastatic patients. For patients with activating EGFR mutations, tyrosine kinase inhibitors are the best treatment choice. NSCLC initially exhibits an excellent response to treatment; however, acquired resistance has been observed in many patients, leading to ineffective treatment. Clinical resistance is an impediment in the treatment of patients with advanced NSCLC. Many sequencing technologies have shown that long non‐coding RNA (lncRNA) is expressed differently between drug‐resistant and drug‐sensitive lung cancer cells. We review the literature on lncRNA in drug resistance of NSCLC. The aim of this review is to gain insight into the molecular mechanisms of drug resistance, mainly focusing on the role of lncRNA in NSCLC.

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Section: Resultsmentioning

confidence: 99%

Role of long non‐coding RNA in drug resistance in non‐small cell lung cancer

Wang

et al. 2018

Thoracic Cancer

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“…Gong et al previously reported that KCNQ1OT1 might promote glioma development by sponging miR-370, 8 the overexpression of which has been found to reduce beta-catenin protein level and transcriptional activity in osteosarcoma cells. 31 LncRNAs interacting with beta-catenin has been demonstrated to prevent beta-catenin degradation, 32,33 and research by Gao et al have shown the KCNQ1OT1-beta-catenin association. 16 In the present research we didn't observe any signicant inuence on beta-catenin protein level in osteosarcoma by KCNQ1OT1 overexpression or knockdown; however, KCNQ1OT1 overexpression signicantly increased beta-catenin's transcriptional activity and reduced beta-catenin Ser37 phosphorylation level, which is one of the initiative steps leading to beta-catenin degradation, while KCNQ1OT1 knockdown showed opposite effects.…”

Section: Discussionmentioning

confidence: 99%

Retracted Article: Long non-coding RNA KCNQ1OT1 promotes osteosarcoma progression by increasing β-catenin activity

Cao

2018

RSC Adv.

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“…Recently, many studies have reported that lncRNAs can play an important role in various biological processes including cell development, proliferation, and migration in cancers. LncRNA BCAR4 can promote colon cancer progression through activating Wnt/β-catenin (Ouyang et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

LINC00968 functions as an oncogene in osteosarcoma by activating the PI3K/AKT/mTOR signaling

Liu

Yuan

Sun

et al. 2018

Journal Cellular Physiology

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Osteosarcoma is recognized as a malignant tumor in the skeletal system. Long non-coding RNAs (lncRNAs) have been exhibited to play crucial roles in osteosarcoma development. Our current study focused on the biological effects and mechanism of LINC00968 in osteosarcoma pathogenesis. We observed that LINC00968 was dramatically elevated in osteosarcoma cells including U2OS, MG63, Saos-2, SW1353, and 143-B cells compared to human osteoblast cell line hFOB. Silence of LINC00968 inhibited osteosarcoma cell growth and proliferation in vitro. Reversely, overexpression of LINC00968 promoted osteosarcoma cell survival and cell colony formation ability in Saos-2 and 143-B cells. In addition, LINC00968 was able to induce osteosarcoma cell migration and invasion through up-regulating MMP-2 and MMP-9 protein levels. The phosphoinosmde-3-kinase/Protein Kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway has been reported to participate in several cancer types. Here, in our study, we found that PI3K/AKT/mTOR pathway was involved in osteosarcoma progression. Knockdown of LINC00968 inactivated PI3K/AKT/mTOR signaling pathway in vitro. Subsequently, in vivo tumor xenografts were established using 143-B cells to investigate whether LINC00968 can induce osteosarcoma development in vivo. Consistently, it was indicated that inhibition of LINC00968 significantly inhibited osteosarcoma progression in vivo. Taken these together, in our research, LINC00968 could be provided as a novel prognostic biomarker and therapeutic target in osteosarcoma diagnosis and treatment.

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LncRNA BCAR4 promotes colon cancer progression via activating Wnt/β-catenin signaling

Cited by 47 publications

References 39 publications

Role of long non‐coding RNA in drug resistance in non‐small cell lung cancer

Role of long non‐coding RNA in drug resistance in non‐small cell lung cancer

Retracted Article: Long non-coding RNA KCNQ1OT1 promotes osteosarcoma progression by increasing β-catenin activity

LINC00968 functions as an oncogene in osteosarcoma by activating the PI3K/AKT/mTOR signaling

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