Long non-coding RNA NORAD promotes pancreatic cancer stem cell proliferation and self-renewal by blocking microRNA-202-5p-mediated ANP32E inhibition

Ma, Yu‐Shui; Yang, Xiaoli; Liu, Yushan; Ding, Hua; Wu, Jianjun; Shi, Yi; Jia, Chengyou; Lu, Gai‐Xia; Zhang, Dandan; Wang, Huimin; Wang, Pei‐Yao; Yu, Fei; Lv, Zhongwei; Wang, Gao‐Ren; Liu, Ji‐Bin; Fu, Da

doi:10.1186/s12967-021-03052-5

Cited by 20 publications

(14 citation statements)

References 43 publications

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“…All the samples had not received medical treatment and/or radiation treatment before surgery. The inclusion and exclusion criteria were according to a previous report [ 17 ]. Immediately after collection, the excised experimental specimens were immersed in an EP tube containing a preservation solution and stored in a −80°C refrigerator.…”

Section: Methodsmentioning

confidence: 99%

“…After culture for 48 h, total RNA was extracted from transfected cells using TRIzol reagent (Beyotime, Shanghai, China) and then reverse-transcribed using the PrimeScript RT reagent kit (KeyGen company, Nanjing, China). The protocols of RT-PCR were according to a previous report [ 17 ]. Each sample was tested in triplicate wells and repeated three times.…”

Section: Methodsmentioning

confidence: 99%

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Solute Carrier Family 35 Member F2 Regulates Cisplatin Resistance and Promotes Malignant Progression of Pancreatic Cancer by Regulating RNA Binding Motif Protein 14

Zhang

Yuan

et al. 2022

Journal of Oncology

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We aimed to explore the role of Solute Carrier Family 35 Member F2 (SLC35F2) in pancreatic cancer (PCa) and to further study whether SLC35F2 regulates cisplatin resistance of PCa cells through the modulation of RNA binding motif protein 14 (RBM14) expression. SLC35F2 expression in 60 pairs of PCa tissues and adjacent ones was studied by RT-PCR analysis. Meanwhile, SLC35F2 expression levels in PCa cell lines were also evaluated by qPCR assay. In addition, SLC35F2 knockdown models were constructed in PCa cisplatin-resistant cells. Furthermore, we determined the interaction between SLC35F2 and RBM14 via luciferase assay. The findings of the present study demonstrated that SLC35F2 was significantly upregulated in PCa tissues. High level of SLC35F2 indicated higher incidence of metastasis and shorter survival rates. In vitro cell experiments revealed that knockdown of SLC35F2 suppressed cell invasion and metastasis capacity of cisplatin-resistant PCa cell lines PANC-1/DDP and CFPAC-1/DDP. It was also suggested that the key protein RBM14 in the SLC35F2 knockdown group was remarkably reduced. SLC35F2 can bind to RBM14 specifically. Overexpression of RBM14 partially reversed the effects of knockdown of SLC35F2 on the development of PCa. SLC35F2 expression in PCa tissues and cell lines is remarkably increased. In addition, it was also suggested that SLC35F2 may regulate cisplatin resistance of PCa cells through modulating RBM14 expression. In conclusion, it is conceivable from the study that SLC35F2 was remarkably upregulated in PCa and promoted the malignancy of PCa via regulating RBM14.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Solute Carrier Family 35 Member F2 Regulates Cisplatin Resistance and Promotes Malignant Progression of Pancreatic Cancer by Regulating RNA Binding Motif Protein 14

Zhang

Yuan

et al. 2022

Journal of Oncology

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“…Therefore, vitamin D3/VDR signaling may prevent acquiring a stem-like phenotype by normal mammary gland progenitors and somatic breast cancer cells ( Figure 2 ). Several pathways involved in cancer stemness are modulated by lncRNAs, and their targeting may be considered a new strategy to control tumor development, invasion, metastasis, and therapeutic resistance (e.g., [ 32 , 33 , 34 ]).…”

Section: Vitamin D Signaling In Breast Cancermentioning

confidence: 99%

Vitamin D May Protect against Breast Cancer through the Regulation of Long Noncoding RNAs by VDR Signaling

Błasiak

Chojnacki

Pawłowska

et al. 2022

IJMS

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Dietary vitamin D3 has attracted wide interest as a natural compound for breast cancer prevention and therapy, supported by in vitro and animal studies. The exact mechanism of such action of vitamin D3 is unknown and may include several independent or partly dependent pathways. The active metabolite of vitamin D3, 1α,25-dihydroxyvitamin D3 (1,25(OH)2D, calcitriol), binds to the vitamin D receptor (VDR) and induces its translocation to the nucleus, where it transactivates a myriad of genes. Vitamin D3 is involved in the maintenance of a normal epigenetic profile whose disturbance may contribute to breast cancer. In general, the protective effect of vitamin D3 against breast cancer is underlined by inhibition of proliferation and migration, stimulation of differentiation and apoptosis, and inhibition of epithelial/mesenchymal transition in breast cells. Vitamin D3 may also inhibit the transformation of normal mammary progenitors into breast cancer stem cells that initiate and sustain the growth of breast tumors. As long noncoding RNAs (lncRNAs) play an important role in breast cancer pathogenesis, and the specific mechanisms underlying this role are poorly understood, we provided several arguments that vitamin D3/VDR may induce protective effects in breast cancer through modulation of lncRNAs that are important for breast cancer pathogenesis. The main lncRNAs candidates to mediate the protective effect of vitamin D3 in breast cancer are lncBCAS1-4_1, AFAP1 antisense RNA 1 (AFAP1-AS1), metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), long intergenic non-protein-coding RNA 511 (LINC00511), LINC00346, small nucleolar RNA host gene 6 (SNHG6), and SNHG16, but there is a rationale to explore several other lncRNAs.

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“…Numerous clinical studies have addressed the role of miR-202 in gastrointestinal tract tumors (GIT), including oral [ 12 ], esophageal [ 19 , 20 , 21 ], gastric [ 22 , 23 , 24 ], pancreatic [ 25 , 26 , 27 , 28 ], hepatocellular [ 29 , 30 , 31 ], and colorectal [ 32 , 33 , 34 , 35 ] cancers, and documented a lower expression of miR-202 in tumor tissues and a tumor suppressive function of miR-202 overexpression on GIT cancer progression. In oral cancer cell lines, overexpression of miR-202 downregulated the protein expression level of the transcription factor Sp1, which, in turn, reduced cancer cell migration and invasion.…”

Section: Mir-202 As a Novel Gastrointestinal Tract Tumor Suppressormentioning

confidence: 99%

“…Pancreatic cancer (PC) is currently rated as the fourth leading cause of cancer-related death worldwide [ 39 ]. A tumor suppressor function for miR-202 in pancreatic carcinoma is suggested by all preclinical and clinical studies up to date [ 25 , 26 , 27 , 28 ]. lncRNA NORAD and ANP32E were upregulated in PC tissues and cells, whereas the miR-202-5p level was down-regulated.…”

Section: Mir-202 As a Novel Gastrointestinal Tract Tumor Suppressormentioning

confidence: 99%

The microRNA-202 as a Diagnostic Biomarker and a Potential Tumor Suppressor

Ahmed

Rajendran

Scherthan

2022

IJMS

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MicroRNA-202 (miR-202) is a member of the highly conserved let-7 family that was discovered in Caenorhabditis elegans and recently reported to be involved in cell differentiation and tumor biology. In humans, miR-202 was initially identified in the testis where it was suggested to play a role in spermatogenesis. Subsequent research showed that miR-202 is one of the micro-RNAs that are dysregulated in different types of cancer. During the last decade, a large number of investigations has fortified a role for miR-202 in cancer. However, its functions can be double-edged, depending on context they may be tumor suppressive or oncogenic. In this review, we highlight miR-202 as a potential diagnostic biomarker and as a suppressor of tumorigenesis and metastasis in several types of tumors. We link miR-202 expression levels in tumor types to its involved upstream and downstream signaling molecules and highlight its potential roles in carcinogenesis. Three well-known upstream long non-coding-RNAs (lncRNAs); MALAT1, NORAD, and NEAT1 target miR-202 and inhibit its tumor suppressive function thus fueling cancer progression. Studies on the downstream targets of miR-202 revealed PTEN, AKT, and various oncogenes such as metadherin (MTDH), MYCN, Forkhead box protein R2 (FOXR2) and Kirsten rat sarcoma virus (KRAS). Interestingly, an upregulated level of miR-202 was shown by most of the studies that estimated its expression level in blood or serum of cancer patients, especially in breast cancer. Reduced expression levels of miR-202 in tumor tissues were found to be associated with progression of different types of cancer. It seems likely that miR-202 is embedded in a complex regulatory network related to the nature and the sensitivity of the tumor type and therapeutic (pre)treatments. Its variable roles in tumorigenesis are mediated in part thought its oncogene effectors. However, the currently available data suggest that the involved signaling pathways determine the anti- or pro-tumorigenic outcomes of miR-202’s dysregulation and its value as a diagnostic biomarker.

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Long non-coding RNA NORAD promotes pancreatic cancer stem cell proliferation and self-renewal by blocking microRNA-202-5p-mediated ANP32E inhibition

Cited by 20 publications

References 43 publications

Solute Carrier Family 35 Member F2 Regulates Cisplatin Resistance and Promotes Malignant Progression of Pancreatic Cancer by Regulating RNA Binding Motif Protein 14

Solute Carrier Family 35 Member F2 Regulates Cisplatin Resistance and Promotes Malignant Progression of Pancreatic Cancer by Regulating RNA Binding Motif Protein 14

Vitamin D May Protect against Breast Cancer through the Regulation of Long Noncoding RNAs by VDR Signaling

The microRNA-202 as a Diagnostic Biomarker and a Potential Tumor Suppressor

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