| [1] PubMed ID: | 32809092 |
| Disease Name: | Endometriosis |
| Sample: | endometrium tissues |
| Dysfunction Pattern: | regulation[PI3K/AKT pathway] |
| Validated Method: | qRT-PCR//MTT//Luciferase Report Assay//Western Blot |
| Description: | Taken together, our study firstly demonstrates that MALAT1 regulates apoptosis of HESCs through miR-126-5p/CREB1 axis mediated PI3K/AKT pathway. |
| Causality: | Yes |
| Causal Description: | Knockdown of MALAT1 or CREB1 restrained proliferation and induced apoptosis as confirmed by upregulating cleaved caspase-3 and Bax, and down-regulating Bcl-2 in HESCs, while inhibition of miR-126-5p presented the opposite results. |
| Clinical-realted Application: | |
| [2] PubMed ID: | 30371869 |
| Disease Name: | Endometriosis |
| Sample: | endometriosis granulosa cells |
| Dysfunction Pattern: | Interaction[ERK/MAPK pathway] |
| Validated Method: | qRT-PCR |
| Description: | We first found that MALAT1 lncRNA was significantly down-regulated in endometriosis GCs and was associated with the antral follicle count (R = 0.376, P < 0.001 versus control).MALAT1 knockdown induced an increase in both the mRNA and protein levels of P21, and of P53, phosphorylated ERK1/2 (p-ERK1/2) and phosphorylated c-Jun N-terminal protein kinase (p-JNK) protein levels, as well as causing a decrease in cyclin dependent kinase 2 (CDK2), cyclin D1 and p-P38 MAPK protein levels. Furthermore, inhibition of the ERK/MAPK pathway with U0126, the up-regulation of p-ERK1/2, P21 and P53, and the down-regulation of CDK2 and cyclin D1 by the knockdown of MALAT1 were all attenuated by MALAT1 knockdown. |
| Causality: | Yes |
| Causal Description: | MALAT1 knockdown in KGN cells inhibited cell proliferation and cell-cycle progression. |
| Clinical-realted Application: | |
| [3] PubMed ID: | 30324652 |
| Disease Name: | Endometriosis |
| Sample: | Endometriosis tissue |
| Dysfunction Pattern: | Expression[highly expressed] |
| Validated Method: | qRT-PCR//MTT//IHC//Western Blot |
| Description: | In the present study, we found that both lncRNA-MALAT1 and autophagy level were up-regulated in ectopic endometrium from patients with endometriosis, and its expression level correlates positively with that of hypoxia-inducible factor-1α (HIF-1α). |
| Causality: | No |
| Causal Description: | |
| Clinical-realted Application: | |
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