acal is a Long Non-coding RNA in JNK Signaling in Epithelial Shape Changes during Drosophila Dorsal Closure

Abstract Background Diabetic nephropathy (DN) is a common complication of diabetes. Long non-coding RNA (lncRNA) cancer susceptibility candidate 2 (CASC2) is reported to exert a protective role in DN by a previous study. The working mechanism underlying the protective role of CASC2 in DN progression was further explored in this study. Methods The expression of CASC2 and microRNA-135a-5p (miR-135a-5p) was determined by real-time quantitative polymerase chain reaction (RT-qPCR). Cell proliferation ability was assessed by Cell Counting Kit-8 (CCK8) assay and 5-ethynyl-29-deoxyuridine (EDU) assay. Enzyme-linked immunosorbent assay (ELISA) was conducted to analyze the production of inflammatory cytokines in the supernatant. Western blot assay was performed to analyze protein expression. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to verify the target relationship between miR-135a-5p and CASC2 or tissue inhibitors of metalloproteinase 3 (TIMP3). Results High glucose (HG) treatment reduced the expression of CASC2 in human glomerular mesangial cells (HMCs) in a time-dependent manner. CASC2 overexpression suppressed HG-induced proliferation, inflammation and fibrosis in HMCs. miR-135a-5p was validated as a target of CASC2, and CASC2 restrained HG-induced influences in HMCs partly by down-regulating miR-135a-5p. miR-135a-5p bound to the 3ʹ untranslated region (3ʹUTR) of TIMP3, and CASC2 positively regulated TIMP3 expression by sponging miR-135a-5p in HMCs. miR-135a-5p silencing inhibited HG-induced effects in HMCs partly by up-regulating its target TIMP3. CASC2 overexpression suppressed HG-induced activation of Jun N-terminal Kinase (JNK) signaling partly through mediating miR-135a-5p/TIMP3 signaling. Conclusions In conclusion, CASC2 alleviated proliferation, inflammation and fibrosis in DN cell model by sponging miR-135a-5p to induce TIMP3 expression.

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The canonical Wg and JNK signaling cascades collaborate to promote both dorsal closure and ventral patterning

Development ◽

10.1242/dev.127.16.3607 ◽

2000 ◽

Vol 127 (16) ◽

pp. 3607-3617 ◽

Cited By ~ 3

Author(s):

D.G. McEwen ◽

R.T. Cox ◽

M. Peifer

Keyword(s):

Cell Fate ◽

Signaling Cascades ◽

Dorsal Closure ◽

Kinase Signaling ◽

Jnk Signaling ◽

Cell Fate Decisions ◽

Wingless Signaling ◽

Kinase Signaling Pathway ◽

Dorsal Epidermis ◽

Shape Changes

Elaboration of the Drosophila body plan depends on a series of cell-identity decisions and morphogenetic movements regulated by intercellular signals. For example, Jun N-terminal kinase signaling regulates cell fate decisions and morphogenesis during dorsal closure, while Wingless signaling regulates segmental patterning of the larval cuticle via Armadillo. wingless or armadillo mutant embryos secrete a lawn of ventral denticles; armadillo mutants also exhibit dorsal closure defects. We found that mutations in puckered, a phosphatase that antagonizes Jun N-terminal kinase, suppress in a dose-sensitive manner both the dorsal and ventral armadillo cuticle defects. Furthermore, we found that activation of the Jun N-terminal kinase signaling pathway suppresses armadillo-associated defects. Jun N-terminal kinase signaling promotes dorsal closure, in part, by regulating decapentaplegic expression in the dorsal epidermis. We demonstrate that Wingless signaling is also required to activate decapentaplegic expression and to coordinate cell shape changes during dorsal closure. Together, these results demonstrate that MAP-Kinase and Wingless signaling cooperate in both the dorsal and ventral epidermis, and suggest that Wingless may activate both the Wingless and the Jun N-terminal kinase signaling cascades.

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Baicalin Protects Against Acute Pancreatitis Involving JNK Signaling Pathway via Regulating miR-15a

The American Journal of Chinese Medicine ◽

10.1142/s0192415x21500087 ◽

2020 ◽

pp. 1-15

Author(s):

Jie Zhen ◽

Wei Chen ◽

Yang Liu ◽

Xuefeng Zang

Keyword(s):

Acute Pancreatitis ◽

Signaling Pathway ◽

Jnk Signaling ◽

Scutellaria Baicalensis Georgi ◽

Cerna Network ◽

Non Coding Rna ◽

Jnk Signaling Pathway ◽

Direct Target ◽

Long Non Coding Rna ◽

Competitive Endogenous Rna

Acute pancreatitis (AP) is a kind of reversible inflammatory process of the exocrine pancreas. During the process, systemic inflammatory syndromes are involved, which relates closely to inflammatory mediators. Baicalin is a type of flavone compound extracted from Scutellaria baicalensis Georgi and exhibits anti-inflammation effect in several cancers. In this study, baicalin displayed a suppressing role on IL-1[Formula: see text], TNF[Formula: see text] and IL-6 in both cell and mice models. Necrosis was decreased in the baicalin treatment group and got a markedly lower pathological score. In this study, miR-15a is the core intermediate in baicalin regulation, which increased through baicalin treatment and protected pancreas cells and tissues, inhibiting the JNK signaling pathway by targeting MAP2K4. The long non-coding RNA MALAT1 is also a direct target of miR-15a and forms a competitive endogenous RNA (ceRNA) network with MAP2K4, which can be regulated by baicalin. In addition, upstream genes, including CDC42 and MAP3K1, were also regulated by baicalin, of which CDC42 was confirmed to form the second ceRNA network with MALAT1 and miR-15a. In conclusion, baicalin exhibits therapeutic activity towards AP by pumping up miR-15a level and inhibiting CDC42/MAP3K1, which affects AP as a brake by targeting MAP2K4 and inhibiting the JNK signaling pathway.

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Innate immune responses and type 1 diabetes: A role for a long non-coding RNA?

Diabetologie und Stoffwechsel ◽

10.1055/s-0034-1374906 ◽

2014 ◽

Vol 9 (S 01) ◽

Author(s):

MP Ashton ◽

I Tan ◽

L Mackin ◽

C Elso ◽

E Chu ◽

...

Keyword(s):

Type 1 Diabetes ◽

Immune Responses ◽

Innate Immune ◽

Innate Immune Responses ◽

Non Coding Rna ◽

Long Non Coding Rna

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Long non-coding RNA CCAT1 is overexpressed in endometrial cancer and regulates growth and transcriptome of endometrial adenocarcinoma cells

10.1055/s-0040-1718183 ◽

2020 ◽

Author(s):

S Schüler-Toprak ◽

M Skrzypczak ◽

F Weber ◽

O Ortmann ◽

O Treeck

Keyword(s):

Endometrial Cancer ◽

Endometrial Adenocarcinoma ◽

Non Coding Rna ◽

Adenocarcinoma Cells ◽

Long Non Coding Rna

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Long non-coding RNA expression profiles in human parathyroid tumors

Endocrine Abstracts ◽

10.1530/endoabs.49.gp130 ◽

2017 ◽

Author(s):

Annamaria Morotti ◽

Irene Forno ◽

Valentina Andre ◽

Andrea Terrasi ◽

Chiara Verdelli ◽

...

Keyword(s):

Expression Profiles ◽

Rna Expression ◽

Parathyroid Tumors ◽

Non Coding Rna ◽

Long Non Coding Rna

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The Variant rs145204276 of GAS5 is Associated with the Development and Prognosis of Gastric Cancer

Journal of Gastrointestinal and Liver Diseases ◽

10.15403/jgld.2014.1121.271.qjl ◽

2018 ◽

Vol 27 (1) ◽

pp. 19-24 ◽

Cited By ~ 7

Author(s):

Qianjun Li ◽

Gang Ma ◽

Huimin Guo ◽

Suhua Sun ◽

Ying Xu ◽

...

Keyword(s):

Gastric Cancer ◽

Survival Rate ◽

Cancer Progression ◽

Regulatory Mechanism ◽

Tumor Stage ◽

Kaplan Meier ◽

Non Coding Rna ◽

Early Tumor ◽

Long Non Coding Rna ◽

Clinicopathological Variables

Background & Aims: Down-regulation of the growth arrest specific transcript 5 (GAS5) (long non-coding RNA) is associated with cell proliferation of gastric cancer (GC) and a poor prognosis. We aimed to investigate whether the variant rs145204276 of GAS5 is associated with the prognosis of GC in the Chinese population, and to unveil the regulatory mechanism underlying the GAS5 expression in GC tissues.Method: 1,253 GC patients and 1,354 healthy controls were included. The frequency of the genotype del/del and the allele del of rs145204276 were compared between the patients and the controls and between different subgroups of patients classified by clinicopathological variables. The overall survival rate was analyzed according to the Kaplan-Meier method using the log-rank test.Results: The frequency of genotype del/del was significantly lower in patients than in the controls (7.0% vs. 9.1%, p = 0.001). Kaplan-Meier analysis showed that genotype del/del was significantly associated with a higher survival rate (p = 0.01). Patients with late tumor stage were found to have a significantly lower rate of genotype del/del than those with an early tumor stage (4.9% vs. 8.8%, p = 0.01). Patients with UICC III and IV were found to have a significantly lower rate of genotype del/del than those with UICC I and II (5.3% vs. 8.1%, p = 0.02).Conclusion: The variant rs145204276 of GAS5 is associated with the development and prognosis of GC. The allele del of rs145204276 is associated with a remarkably lower incidence of cancer progression and metastasis.

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