Long non‑coding RNA MLK7‑AS1 promotes proliferation in human colorectal cancer via downregulation of p21 expression

Zhang, Rui; Li, Jibin; Yan, Xiaofei; Jin, Keer; Li, Wenya; Liu, Xin; Zhao, Jianfeng; Shang, Wen; Zhao, Xiaojun

doi:10.3892/mmr.2018.9702

Cited by 7 publications

(4 citation statements)

References 51 publications

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“…p21 is a crucial regulator of cell cycle progression and serves an important role in tumorigenesis and is regarded as a tumor suppressive protein. Numerous studies have reported that the downregulation of p21 is involved in a number of human cancers and is associated with cell proliferation (38,39). p21 may also act independently or with other cell cycle regulators, such as the CDK4/6 complex and p53 (13).…”

Section: Discussionmentioning

confidence: 99%

Suppression of CDCA3 inhibits prostate cancer progression via NF‑κB/cyclin D1 signaling inactivation and p21 accumulation

Zhang

Zhu

et al. 2021

Oncol Rep

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Dysregulation of the cell cycle contributes to tumor progression. Cell division cycle-associated 3 (CDCA3) is a known trigger of mitotic entry and has been demonstrated to be constitutively upregulated in tumors. It is therefore associated with carcinogenic properties reported in various cancers. However, the role of CDCA3 in prostate cancer is unclear. In the present study, western blotting and analysis of gene expression profiling datasets determined that CDCA3 expression was upregulated in prostate cancer and was associated with a poor prognosis. CDCA3 knockdown in DU145 and PC-3 cells led to decreased cell proliferation and increased apoptosis, with increased protein expression levels of cleaved-caspase3. Further experiments demonstrated that downregulated CDCA3 expression levels induced G0/G1 phase arrest, which was attributed to increased p21 protein expression levels and decreased cyclin D1 expression levels via the regulation of NF-κB signaling proteins (NFκB-p105/p50, IKKα/β, and pho-NFκB-p65). In conclusion, these results indicated that CDCA3 may serve a crucial role in prostate cancer and consequently, CDCA3 knockdown may be used as a potential therapeutic target.

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Section: Discussionmentioning

confidence: 99%

Suppression of CDCA3 inhibits prostate cancer progression via NF‑κB/cyclin D1 signaling inactivation and p21 accumulation

Zhang

Zhu

et al. 2021

Oncol Rep

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“…Previous data supports the hypothesis that targeting apoptosis may be a promising and protective strategy for the management of colorectal cancer. MLK7-AS1 knockdown promoted CRC cell apoptosis in vitro (28). Lupeol-induced cellular apoptosis of both colorectal cancer cell lines, which increased p53 and decreased Bcl2 protein levels (29).…”

Section: Discussionmentioning

confidence: 99%

Knockdown of KLK12 inhibits viability and induces�apoptosis in human colorectal cancer HT-29 cell line

Zhou

Fang

et al. 2019

Int J Mol Med

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Kallikrein-related peptidase 12 (KLK12) is overexpressed in cancer tissues including gastric, breast and prostate cancer. However, the role of KLK12 in colorectal cancer is not fully understood. In the present study, the level of KLK12 was determined by performing reverse transcription-polymerase chain reaction (RT-qPcR) in colorectal cancer tissues and cell lines. Lipofectamine ® 2000 was used to transfect HT-29 cells to overexpress and knockdown KLK12. cell viability, migration, invasion and apoptosis were detected by MTT, wound healing, Transwell and flow cytometry assays, respectively. The mRNA and protein expression levels of EMT-associated proteins, apoptosis-associated proteins, phosphorylated adenosine monophosphate-activated protein kinase (p-AMPK) and phosphorylated mammalian target of rapamycin (p-mTOR) were determined by RT-qPcR and western blot analysis. It was identified that the KLK12 mRNA levels were increased significantly in colorectal cancer tissues and cell lines. KLK12 small interfering RNA inhibited cell viability, migration and invasion. Furthermore, epithelial-mesenchymal transition (EMT)-associated proteins were altered by siKLK12. cell apoptosis was induced by KLK12 downregulation, which was demonstrated by the changes in apoptosis-associated proteins; however, KLK12 overexpression produced the opposite effect. SiKLK12 enhanced the expression of p-AMPK and suppressed the expression of p-mTOR, while KLK12 overexpression had the opposite effect. Promotion of KLK12 overexpression-induced cell viability was reversed by 5-aminoimidazole-4-carboxamide ribonucleotide, an activator of the AMPK signaling pathway, and rapamycin, a specific inhibitor of the mTOR signaling pathway. Taken together, the results of the present study indicated that KLK12 was overexpressed in colorectal cancer and may regulate cell behavior, potentially via the AMPK and mTOR pathways.

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“…Meanwhile, the increased MLK7-AS1 expression was positively correlated to a series of clinicopathological factors in patients with CRC. 28 Li et al reported that long noncoding RNA FGD5 antisense RNA 1 (FGD5-AS1) was increased in CRC cells9. 29 However, the molecular mechanisms of lncRNAs in CRC progression have not been fully understood yet.…”

Section: Discussionmentioning

confidence: 99%

LncRNA BLACAT1/miR-519d-3p/CREB1 Axis Mediates Proliferation, Apoptosis, Migration, Invasion, and Drug-Resistance in Colorectal Cancer Progression

Chen¹,

Zhou²,

Chen³

et al. 2020

CMAR

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Background Colorectal cancer (CRC) is a common severe disease around the world. The merging papers reported that long noncoding RNAs (lncRNAs) took part in the diversified pathological processes of CRC. This study aimed to uncover the role and the potential mechanism of lncRNA bladder cancer-associated transcript 1 (BLACAT1) in CRC progression. Methods LncRNA BLACAT1, micro-519d-3p (miR-519d-3p), and cAMP-responsive element binding protein 1 ( CREB1 ) levels were detected by quantitative real-time polymerase chain reaction (qRT-PCR) in CRC tissues and cells. The bio-functional effects were examined by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), flow cytometry assay, and transwell assay. The susceptibility testing was determined by oxaliplatin (OXA) administration. The potential binding sites between miR-519d-3p and BLACAT1 or CREB1 were predicted by online software starBase and confirmed by dual-luciferase reporter analysis. The relative proteins expression in CRC cells was determined by Western blot analysis. Xenograft tumor model was used to evaluate biological function of BLACAT1 in vivo. Results The expression of BLACAT1 was promoted in CRC tissues and cells, and correlated to the TNM (tumor, node, metastasis) stage, distant metastasis, and overall survival rate. Silencing of BLACAT1 limited the proliferation, migration, and invasion, facilitated the apoptosis, and re-sensitized OXA-resistance in CRC cells. MiR-519d-3p was a target of BLACAT1. Furthermore, miR-519d-3p deletion reversed the positive effects of BLACAT1 deletion on CRC cells. Moreover, our data showed that miR-519d-3p directly targeted CREB1 and BLACAT1 sponged miR-519d-3p to regulate CREB1 expression. Besides, CREB1 disrupted the bio-functional results above from BLACAT1 suppression. Additionally, BLACAT1 knockdown promoted CRC cells sensitivity to OXA in vivo. Conclusion BLACAT1 mediated the progression of CRC and OXA-resistance by miR-519d-3p/ CREB1 axis.

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Long non‑coding RNA MLK7‑AS1 promotes proliferation in human colorectal cancer via downregulation of p21 expression

Cited by 7 publications

References 51 publications

Suppression of CDCA3 inhibits prostate cancer progression via NF‑κB/cyclin D1 signaling inactivation and p21 accumulation

Suppression of CDCA3 inhibits prostate cancer progression via NF‑κB/cyclin D1 signaling inactivation and p21 accumulation

Knockdown of KLK12 inhibits viability and induces�apoptosis in human colorectal cancer HT-29 cell line

LncRNA BLACAT1/miR-519d-3p/CREB1 Axis Mediates Proliferation, Apoptosis, Migration, Invasion, and Drug-Resistance in Colorectal Cancer Progression

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