2020
DOI: 10.1016/j.mce.2020.110887
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LncRNA SNHG4 promotes the increased growth of endometrial tissue outside the uterine cavity via regulating c-Met mediated by miR-148a-3p

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Cited by 17 publications
(19 citation statements)
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“…Besides, Liu et al . found that the reduced abundance level of miR-148a-3p leads to the higher abundance level of its target gene, the small nucleolar RNA host gene 4 ( SNHG4 ), and thus has a direct influence on the ectopic growth of the endometrium outside the uterus 32 . As for miR-28-5p, Vanhie et al .…”
Section: Discussionmentioning
confidence: 99%
“…Besides, Liu et al . found that the reduced abundance level of miR-148a-3p leads to the higher abundance level of its target gene, the small nucleolar RNA host gene 4 ( SNHG4 ), and thus has a direct influence on the ectopic growth of the endometrium outside the uterus 32 . As for miR-28-5p, Vanhie et al .…”
Section: Discussionmentioning
confidence: 99%
“…In ACI [ 20 ], NP [ 30 ], DR [ 19 ], AML [ 21 ], neuroblastoma [ 33 ], CRC [ 35 ], cervical cancer (CC) [ 80 ], non-small-cell lung cancer (NSCLC) [ 28 ], and endometriosis [ 81 ], researchers explored the expression of SNHG4 in patients with these diseases. However, they did not seem to have studied the relationship between SNHG4 and the clinical features of these diseases, nor have they explored the relationship between SNHG4 and disease prognosis.…”
Section: Snhg4 In Human Studiesmentioning
confidence: 99%
“…Similarly, SNHG4 knockdown could inhibit RCC [ 32 ], CRC [ 35 ], osteosarcoma [ 71 ], CC [ 80 ], lung cancer [ 82 ], and NSCLC [ 28 ] tumour growth. In addition, Liu and colleagues [ 81 ] pointed out that silencing SNHG4 inhibited the growth of endometrial tissue outside the uterine cavity in vivo . In summary, the results of in vivo studies showed that SNHG4 not only plays a tumorigenic role in some cancers but also promotes the growth of intimal tissues in non-tumour diseases such as endometriosis.…”
Section: Snhg4 In In Vivo Studiesmentioning
confidence: 99%
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“…The inhibitor of miR-148a-3p combined with SNHG4 knockdown rescued endometriotic lesions growth and upregulated the MET expression. The authors postulated that SNHG4 might upregulate proto-oncogene expression, in particular MET, via the suppression of miR-148a-3p, to promote the increased growth of endometrial tissue outside the uterine cavity and endometriosis lesions [ 110 ]. The impact of oncogenes and the manipulation of oncogenes in therapy for endometriosis deserves future study, particularly as non-hormonal therapies.…”
Section: Therapeutic Opportunities For Lncrnasmentioning
confidence: 99%