miR-582-5p inhibits migration and chemo-resistant capabilities of colorectal cancer cells by targeting TNKS2

Xiao, Weixing; Zhou, Haijun; Chen, Bingrong; Shen, Bin; Zhou, Jun

doi:10.1007/s13258-021-01141-9

Cited by 7 publications

(7 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this study, it was the first time to unveil that miR-582-5p had binding sites with F2RL2. miR-582-5p is widely proved to have a suppressing effect on tumors such as osteosarcoma, bladder cancer, AML, and colorectal cancer [11][12][13][14]. Besides, the low expression level of miR-582-5p appeared in hepatic ischemia/reperfusion injury [15].…”

Section: Discussionmentioning

confidence: 99%

“…miR-582-5p has a strong inhibiting effect on various cancers. For instance, miR-582-5p suppresses the growth and invasion of osteosarcoma cells through targeting NOVA1 [ 11 ], inhibits bladder cancer-genesis through downregulating TTK expression [ 12 ], serves as an antioncogenic biomarker in acute myeloid leukemia (AML), hinders leukemia cell proliferation, induces cell apoptosis [ 13 ], and also hampers the migration and chemoresistant capabilities of colorectal cancer cells through targeting TNKS2 [ 14 ]. In addition, in hepatic ischemia/reperfusion injury, miR-582-5p is discovered to be lowly expressed [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

lncRNA NEAT1 Downregulation Ameliorates the Myocardial Infarction of Mice by Regulating the miR-582-5p/F2RL2 Axis

Bai

et al. 2022

Cardiovascular Therapeutics

View full text Add to dashboard Cite

Background. This study is aimed at effectively investigating the role of coagulation factor II thrombin receptor like 2 (F2RL2) in myocardial infarction (MI) as well as the upstream regulatory miRNA and lncRNA. Methods. Regulatory genes of F2RL2 were analyzed using StarBase and verified by dual-luciferase reporter assay. The MI mouse model was established. The left ventricular ejection fraction (EF) and fractional shortening (FS) were examined by echocardiography. The infarct area, pathological changes, and cell apoptosis in mouse myocardial tissue were evaluated using triphenyltetrazolium chloride and Evans blue, hematoxylin-eosin, and TUNEL staining assays. Oxygen-glucose deprivation- (OGD-) induced human cardiac myocytes (HCMs) were cultured and transfected. The cell viability, proliferation, and apoptosis were determined by CCK-8, EdU staining, and flow cytometry assays. The expressions of F2RL2, miR-582-5p, and nuclear paraspeckle assembly transcript 1 (NEAT1) in myocardial tissues and HCMs were quantified by qRT-PCR or Western blot. Results. NEAT1 sponged miR-582-5p which targeted F2RL2. NEAT1 and F2RL2 were highly expressed while miR-582-5p was lowly expressed in MI mice. F2RL2 downregulation prevented the reduction in EF and SF and the elevation in infarct area and cell apoptosis of MI mice. Both F2RL2 and NEAT1 downregulations reversely modulated the decreased viability and proliferation and the increased apoptosis of OGD-induced HCMs, while miR-582-5p inhibitor did oppositely. NEAT1 silencing upregulated miR-582-5p level but downregulated F2RL2 level. miR-582-5p inhibitor upregulated the F2RL2 level. The role of NEAT1 silencing in OGD-induced HCMs was reversed by miR-582-5p inhibitor whose effect was further offset by F2RL2 downregulation. Conclusion. NEAT1 downregulation ameliorates MI by regulating the miR-582-5p/F2RL2 axis, providing novel biomarkers for MI treatment.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

lncRNA NEAT1 Downregulation Ameliorates the Myocardial Infarction of Mice by Regulating the miR-582-5p/F2RL2 Axis

Bai

et al. 2022

Cardiovascular Therapeutics

View full text Add to dashboard Cite

show abstract

“…In CRC, for example, miR‐4463 acts as an oncogene by promoting the progression of CRC via regulation of the PPP1R12B gene 12 . It has also been proposed that upregulation of miR‐582‐5p expression could inhibit migration and chemotherapy drug resistance of CRC cells 13 . Conversely, several studies have suggested that miR‐506‐3p expression is remarkably lower in CRC cells than in normal cells, suggesting a role as a tumor suppressor in the progression of CRC 14,15 .…”

Section: Introductionmentioning

confidence: 99%

“…12 It has also been proposed that upregulation of miR-582-5p expression could inhibit migration and chemotherapy drug resistance of CRC cells. 13 Conversely, several studies have suggested that miR-506-3p expression is remarkably lower in CRC cells than in normal cells, suggesting a role as a tumor suppressor in the progression of CRC. 14,15 Our preliminary results indicate that miR-506-3p level was decreased in CRC tissues.…”

mentioning

confidence: 99%

Circ‐MALAT1 accelerates cell proliferation and epithelial mesenchymal transformation of colorectal cancer through regulating miR‐506‐3p/KAT6B axis

Yang,

Gong,

Qiu

2023

The Kaohsiung J of Med Scie

View full text Add to dashboard Cite

Colorectal cancer (CRC) is a prevalent malignant tumor of the digestive tract. Circular RNAs may play important roles in the progression of CRC. In this study, we investigated the roles and mechanisms of action of circ‐MALAT1 in CRC. Gene expression and protein abundance were determined using qRT‐PCR and western blot, respectively. Cell proliferation and migration were assessed by MTT, clone formation, and wound‐healing assays. The interactions among the long non‐coding RNA metastasis‐associated lung adenocarcinoma transcript 1 (circ‐MALAT1), miR‐506‐3p, and lysine acetyltransferase 6B (KAT6B) were predicted using the StarBase software and confirmed by the luciferase activity assay. Circ‐MALAT1 and KAT6B were upregulated, while miR‐506‐3p was downregulated in CRC cells. We validated that knocking down of circ‐MALAT1 suppressed proliferation, migration, and epithelial–mesenchymal transition (EMT) of CRC cells, and these effects were abolished by miR‐506‐3p downregulation or KAT6B sufficiency. Our study suggests that circ‐MALAT1 could sponge miR‐506‐3p to regulate the expression of KAT6B. Moreover, KAT6B sufficiency could neutralize miR‐506‐3p‐dependent growth arrest, migration, and EMT. Circ‐MALAT1 promotes cell proliferation, migration, and EMT of CRC cells via the miR‐506‐3p/KAT6B axis, thereby acting as a novel potential therapeutic target for the treatment of colorectal cancer.

show abstract

“…MiRNAs are small noncoding RNAs and have been characterized to regulate chemoresistance [15]. In CRC, miR-582-5p possessed the abilities to repress the migration and chemoresistance of CRC by interacting with TNKS2 [16]. MiR-454-3p facilitated the resistance of CRC to oxaliplatin by targeting PTEN [17].…”

Section: Introductionmentioning

confidence: 99%

LncRNA SNHG11 enhances bevacizumab resistance in colorectal cancer by mediating miR-1207-5p/ABCC1 axis

et al. 2022

View full text Add to dashboard Cite

Long noncoding RNAs (lncRNAs) have been reported to serve as vital regulators in the chemoresistance of human cancers, including colorectal cancer (CRC). In this study, we aimed to explore the functions of lncRNA small nucleolar RNA host gene 11 (SNHG11) in the resistance of CRC to bevacizumab. Quantitative real-time PCR, western blot assay or immunohistochemistry assay were performed to examine the expression of SNHG11, microRNA-1207-5p (miR-1207-5p), ATP binding cassette subfamily C member 1 (ABCC1) and Ki67. Cell Counting Kit-8 assay was conducted to evaluate bevacizumab resistance and cell viability. 5′-ethynyl-2′-deoxyuridine analysis, flow cytometry analysis and wound-healing assay were conducted for cell proliferation, apoptosis and migration, respectively. Dual-luciferase reporter assay and RNA immunoprecipitation assay were employed to analyze the relations among SNHG11, miR-1207-5p and ABCC1. Murine xenograft model assay was employed to analyze bevacizumab resistance in vivo. The exosomes were observed under transmission electron microscopy. SNHG11 was overexpressed in bevacizumab-resistant CRC tissues and cells. Knockdown of SNHG11 restrained bevacizumab resistance, repressed cell proliferation and migration, and promoted apoptosis in bevacizumab-resistant CRC cells. MiR-1207-5p served as the target of SNHG11 and SNHG11 regulated bevacizumab resistance by targeting miR-1207-5p. ABCC1 was the target gene of miR-1207-5p. Overexpression of miR-1207-5p inhibited bevacizumab resistance and cell progression in bevacizumab-resistant CRC cells, with ABCC1 elevation abrogated the impacts. SNHG11 silencing repressed bevacizumab resistance in vivo. In addition, exosomal SNHG11 was upregulated in bevacizumab-resistant CRC cells. SNHG11 contributes to bevacizumab resistance in CRC depending on the modulation of miR-1207-5p and ABCC1.

show abstract

miR-582-5p inhibits migration and chemo-resistant capabilities of colorectal cancer cells by targeting TNKS2

Cited by 7 publications

References 27 publications

lncRNA NEAT1 Downregulation Ameliorates the Myocardial Infarction of Mice by Regulating the miR-582-5p/F2RL2 Axis

lncRNA NEAT1 Downregulation Ameliorates the Myocardial Infarction of Mice by Regulating the miR-582-5p/F2RL2 Axis

Circ‐MALAT1 accelerates cell proliferation and epithelial mesenchymal transformation of colorectal cancer through regulating miR‐506‐3p/KAT6B axis

LncRNA SNHG11 enhances bevacizumab resistance in colorectal cancer by mediating miR-1207-5p/ABCC1 axis

Contact Info

Product

Resources

About