Long non-coding RNA MT1JP exerts anti-cancer effects in breast cancer cells by regulating miR-92-3p

H, Wu; Li, Sa

doi:10.4149/gpb_2019039

Cited by 8 publications

(3 citation statements)

References 37 publications

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“…In breast cancer cells, MT1JP repressed oncogenesis and reversed cisplatin resistance through sponging miR-24-3p and inhibiting the Wnt/b-catenin (47). Consistently, MT1JP exhibited tumor suppressive functions via sponging miR-92-3p and targeting miR-214/RUNX3 axis in breast cancer cells (48,49). In lung cancer cells, MT1JP blocked cell proliferation, migration and invasion through modulation of miR-423-3p/Bim axis (50).…”

Section: Lncrna Mt1jp Regulates Fbxw7mentioning

confidence: 70%

The functions of long noncoding RNAs on regulation of F-box proteins in tumorigenesis and progression

et al. 2022

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Accumulated evidence has revealed that F-box protein, a subunit of SCF E3 ubiquitin ligase complexes, participates in carcinogenesis and tumor progression via targeting its substrates for ubiquitination and degradation. F-box proteins could be regulated by cellular signaling pathways and noncoding RNAs in tumorigenesis. Long noncoding RNA (lncRNA), one type of noncoding RNAs, has been identified to modulate the expression of F-box proteins and contribute to oncogenesis. In this review, we summarize the role and mechanisms of multiple lncRNAs in regulating F-box proteins in tumorigenesis, including lncRNAs SLC7A11-AS1, MT1JP, TUG1, FER1L4, TTN-AS1, CASC2, MALAT1, TINCR, PCGEM1, linc01436, linc00494, GATA6-AS1, and ODIR1. Moreover, we discuss that targeting these lncRNAs could be helpful for treating cancer via modulating F-box protein expression. We hope our review can stimulate the research on exploration of molecular insight into how F-box proteins are governed in carcinogenesis. Therefore, modulation of lncRNAs is a potential therapeutic strategy for cancer therapy via regulation of F-box proteins.

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Section: Lncrna Mt1jp Regulates Fbxw7mentioning

confidence: 70%

The functions of long noncoding RNAs on regulation of F-box proteins in tumorigenesis and progression

et al. 2022

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“…The hippocampal neurons were seeded into a 96-well plate at a density of 1,000/well, grown for 5 days and divided into the following groups: i) Control group (25 mmol/l glucose); ii) HG group (45 mmol/l glucose); iii) HG + low-dose blank serum group (45 mmol/l glucose + 10% total volume of low-dose blank serum); iv) HG + medium-dose blank serum group (45 mmol/l glucose + 10% total volume of medium-dose blank serum); v) HG + high-dose blank serum group (45 mmol/l glucose + 10% total volume of high-dose blank serum); vi) HG + low-dose green tea serum group (45 mmol/l glucose + 10% total volume of low-dose green tea serum); vii) HG + middle-dose green tea serum group (45 mmol/l glucose + 10% total volume of medium-dose green tea serum); viii) HG + high-dose green tea serum group (45 mmol/l glucose + 10% total volume of high-dose green tea serum); ix) HG + SP group [45 mmol/l glucose + 10 µmol/l SP600125 (JNK inhibitor; Sigma-Aldrich; Merck KGaA)]; and x) HG + ML-7 group [45 mmol/l glucose + 10 µmol/l ML-7 (MLCK inhibitor; Sigma-Aldrich; Merck KGaA)]. Cellular activity was assessed using Cell Counting Kit-8 (CCK-8) assays according to a previous study (25). Briefly, 10 µl CCK-8 solution (cat.…”

Section: High-performance Liquid Chromatography (Hplc)mentioning

confidence: 99%

Green tea protects against hippocampal neuronal apoptosis in diabetic encephalopathy by inhibiting JNK/MLCK signaling

Liu

Zhū

et al. 2021

Mol Med Rep

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Although diabetic encephalopathy (DE) is a major late complication of diabetes, the pathophysiology of postural instability in DE remains poorly understood. Prior studies have suggested that neuronal apoptosis is closely associated with cognitive function, but the mechanism remains to be elucidated. Green tea, which is a non-fermented tea, contains a number of tea polyphenols, alkaloids, amino acids, polysaccharides and other components. Some studies have found that drinking green tea can reduce the incidence of neurodegenerative diseases and improve cognitive dysfunction. We previously found that myosin light chain kinase (MLCK) regulates apoptosis in high glucose-induced hippocampal neurons. In neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease, activation of the JNK signaling pathway promotes neuronal apoptosis. However, the relationship between JNK and MLCK remains to be elucidated. Green tea serum was obtained using seropharmacological methods and applied to hippocampal neurons. In addition, a type 1 diabetes rat model was established and green tea extract was administered, and the Morris water maze test, Cell Counting Kit-8 assays, flow cytometry, western blotting and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labelling assays were used to examine the effects of green tea on hippocampal neuronal apoptosis in diabetic rats. The results demonstrated that green tea can protect against hippocampal neuronal apoptosis by inhibiting the JNK/MLCK pathway and ultimately improves cognitive function in diabetic rats. The present study provided novel insights into the neuroprotective effects of green tea.

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“…MT1JP was also reported to inhibit biological activities of breast cancer cells in vitro and in vivo by regulating the miRNA-214/RUNX3 axis. MT1JP acts as a tumor suppressor by regulating miR-92-3p in breast cancer cells [ 15 ]. However, the function of MT1JP in TNBC is still unknown.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA (lncRNA) metallothionein 1 J, pseudogene (MT1JP) is downregulated in triple-negative breast cancer and upregulates microRNA-138 (miR-138) to downregulate hypoxia-inducible factor-1α (HIF-1α)

et al. 2022

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Triple-negative breast cancer (TNBC) is a highly invasive subtype of breast cancer. This study explored the molecular mechanism and influences of metallothionein 1 J, pseudogene (MT1JP), microRNA-138 (miR-138), and hypoxia-inducible factor-1α (HIF-1α) on TNBC cell proliferation and migration. We confirmed TNBC cases by immunohistochemistry (IHC) staining. The expression of MT1JP in two types of tissue collected from 78 TNBC patients was detected by performing real-time quantitative fluorescence PCR (RT-qPCR). To further evaluate the relationship among MT1JP, miR-138 and HIF-1α, expression vectors of MT1JP and HIF-1α, as well as miR-138 mimic and inhibitor, were delivered into BT-549 cells. We observed that MT1JP was downregulated in TNBC. MT1JP was positively correlated with miR-138 but negatively correlated with HIF-1α in TNBC tissues. In TNBC cells, upregulation of miR-138 and downregulation of HIF-1α were observed after overexpression of MT1JP. In addition, overexpression of miR-138 resulted in downregulation of HIF-1α but did not affect the expression of MT1JP. Decreased proliferation rate of TNBC cells was observed after overexpression of MT1JP and miR-138. HIF-1α increased cell proliferation and migration. HIF-1α also suppressed the role of MT1JP and miR-138 in TNBC cell proliferation and migration. In conclusion, our findings demonstrated that MT1JP inhibited TNBC by regulating the miR-138/HIF-1α axis, indicating that MT1JP might serve as a biomarker or target for TNBC treatment.

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Long non-coding RNA MT1JP exerts anti-cancer effects in breast cancer cells by regulating miR-92-3p

Cited by 8 publications

References 37 publications

The functions of long noncoding RNAs on regulation of F-box proteins in tumorigenesis and progression

The functions of long noncoding RNAs on regulation of F-box proteins in tumorigenesis and progression

Green tea protects against hippocampal neuronal apoptosis in diabetic encephalopathy by inhibiting JNK/MLCK signaling

Long noncoding RNA (lncRNA) metallothionein 1 J, pseudogene (MT1JP) is downregulated in triple-negative breast cancer and upregulates microRNA-138 (miR-138) to downregulate hypoxia-inducible factor-1α (HIF-1α)

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