The role of the long non‐coding RNA TDRG1 in epithelial ovarian carcinoma tumorigenesis and progression through miR‐93/RhoC pathway

Chen, Shuo; Wang, Lili; Sun, Kaixuan; Xiu, Yin-Ling; Zong, Zhi‐Hong; Chen, Xi; Zhao, Yang

doi:10.1002/mc.22749

Cited by 21 publications

(26 citation statements)

References 26 publications

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“…Abnormal lncRNA levels can affect the cellular growth, migration, invasion, and cell cycle distribution of trophoblast cells to induce the occurrence and development of PE . There is evidence that TDRG1 is significantly overexpressed in epithelial ovarian cancer or endometrial cancer tissues, promoting cancer cell viability, invasion, and migration and inhibiting apoptosis . In this study, we found that TDRG1 was significantly down‐regulated in the placental tissues of PE patients, and we speculated that TDRG1 levels might be associated with PE development and progression.…”

Section: Discussionmentioning

confidence: 57%

LncRNA TDRG1/miR‐214‐5p axis affects preeclampsia by modulating trophoblast cells

Gong

Cheng

Shi

et al. 2019

Cell Biochemistry & Function

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Because of limited treatment options, preeclampsia (PE) is the leading cause of perinatal morbidity and mortality worldwide. Recently, lncRNA TDRG1 is reported to be aberrantly down-regulated in PE placenta, and the abnormal expression of TDRG1 might play a key or partial role in PE development. In this study, we found that TDRG1 was significantly down-regulated in PE placenta compared with the normal placenta.The cell proliferation, migration, invasion, and cell cycle were explored by CCK-8, wound-healing, transwell, and flow cytometer assay, respectively. Experimental results showed that TDRG1 accelerated the proliferation, migration, and invasion of trophoblast cells. Dual-luciferase reporter assays confirmed that TDRG1 could bind to miR-214-5p. Besides, knockdown of TDRG1 suppressed the cell proliferation, migration, and invasion, while knockdown of miR-214-5p reversed the effect. Jagged1 and Notch1 were negatively regulated by miR-214-5p while positively modulated by TDRG1. In conclusion, TDRG1 promoted trophoblast cells viability and invasion by negatively regulating miR-214-5p expression, contributing to a better understanding of PE pathogenesis and providing new light on TDRG1-directed diagnosis and treatment.Significance of the study: In this work, we observed that TDRG1 was able to promote cell proliferation, migration, and invasion cells by suppressing the expression of miR-214-5p and regulating the Notch signalling pathway in trophoblast cells. As far as we know, the effect of TDRG1/miR-214-5p axis on cell viability, migration, and invasion of trophoblast cells was firstly introduced. Our findings provided a better understanding of the mechanism of PE. Moreover, it is reasonable to believe that TDRG1 may be employed as a strategy to treat PE in the future. K E Y W O R D SmiR-214-5p, Notch1, preeclampsia, TDRG1, trophoblast cells

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Section: Discussionmentioning

confidence: 57%

LncRNA TDRG1/miR‐214‐5p axis affects preeclampsia by modulating trophoblast cells

Gong

Cheng

Shi

et al. 2019

Cell Biochemistry & Function

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“…It exclusively expressed in the testis in non-reproductive tissues, and plays a major role in regulating human spermatogenesis and sperm motility [8, 9]. With the in-depth research, TDRG1 was considered as a key regulator in reproductive organ related cancer such as testicular germ cell tumors (TGCT) [10, 32, 33], epithelial ovarian carcinoma [11] and endometrial carcinoma [12]. Down-regulated expression of TDRG1 reduced the biological activity of TGCT cells [10], and enhanced proliferation and migration of seminoma cells through modulation of the PI3 K/Akt/mTOR signaling pathway and mitochondria-mediated apoptotic pathway [32, 33].…”

Section: Discussionmentioning

confidence: 99%

“…Down-regulated expression of TDRG1 reduced the biological activity of TGCT cells [10], and enhanced proliferation and migration of seminoma cells through modulation of the PI3 K/Akt/mTOR signaling pathway and mitochondria-mediated apoptotic pathway [32, 33]. Furthermore, as a lncRNA, TDRG1 enhanced tumorigenicity by inhibiting the miR-93/RhoC pathway in epithelial ovarian carcinoma [11] and promoted endometrial carcinoma cell development and invasion by positively targeting VEGF-A in endometrial carcinoma [12]. However, there is no evidence that TDRG1 involved in regulation of the pathological process in CC.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, TDRG1 was able to enhance the CC cells growth, migration and invasion. Similarly, the expression of TDRG1 was highly expressed in cancerous tissues and acted as an oncogene to activate tumor cells proliferation and invasion in above productive organ related cancer [11, 12, 32]. On the basis, TRDG1 acts as an oncogene and promoter in CC and can be considered as a novel potential therapeutic target.…”

Section: Discussionmentioning

confidence: 99%

“…TDRG1 was initially considered as a key regulator in sperm motility [9], and was involved in the development and progression of testicular germ cell tumors [10]. Further, as a lncRNA, TDRG1 plays important role in cell proliferation, migration and invasion in epithelial ovarian carcinoma [11] and endometrial carcinoma [12]. Based on these findings, TDRG1 has been considered as a critical modulator in several reproductive organ-related cancers, however, the role and potential mechanism of TDRG1 in the tumorigenesis and progression of CC has not been fully investigated.…”

Section: Introductionmentioning

confidence: 99%

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The lncRNA TDRG1 promotes cell proliferation, migration and invasion by targeting miR-326 to regulate MAPK1 expression in cervical cancer

et al. 2019

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Background Recently, lncRNA-Testis developmental related gene 1 (TDRG1) was proved to be a key modulator in reproductive organ-related cancers. The biological role of TDRG1 in cervical cancer (CC) progression remains largely unknown. Method Real-time PCR (qRT-PCR) examined the expression level of TDRG1, microRNA (miR)-326 and MAPK1 mRNA. OS tissues and corresponding relative normal tissues, as well as CC cell lines and normal cell line Ect1/E6E7 were collected to determine the expression of TDRG1 in CC. MTT, colony formation, wound-healing, transwell and flow cytometer assay detected the influence of TDRG1 and miR-326 on CC cells growth, metastasis and apoptosis. Western blot examined proteins level. Bioinformatics, RNA pull-down assay, RNA immunoprecipitation and dual-luciferase reporter assays detected the molecular mechanism of TDRG1 in CC. Xenograft tumour model was established to determine the role of TDRG1 in vivo. Results The expression of TDRG1 was significantly increased in CC tissues and cell lines compared with normal tissue and normal cell line respectively and its expression was associated with clinicopathological characteristics of CC patients. Knockdown of TDRG1 inhibited the cell proliferation, migration and invasion in Hela and SIHA cells. Moreover, TDRG1 directly interacted with miR-326, and the inhibition effect on cell growth and metastasis induced by TDRG1 siRNA can be abrogated by miR-326 silencing by its inhibitor in Hela and SIHA cells. Further, MAPK1 was proved to be a direct target of miR-326, and its expression was negatively regulated by miR-326 while positively modulated by TDRG1. Conclusion TDRG1 acts as a competing endogenous lncRNA (ceRNA) to modulate MAPK1 by sponging miR-326 in CC, shedding new light on TDRG1-directed diagnostics and therapeutics in CC.

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Long non‐coding RNA SNHG1 stimulates ovarian cancer progression by modulating expression of miR‐454 and ZEB1

Zhu

Yan

et al. 2021

Molecular Oncology

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Ovarian cancer (OC) is highly prevalent and is associated with high mortality rates due to metastasis and relapse. In this study, we assessed the role of long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) in OC to gain further insight into mechanisms that contribute to its aggressiveness. We analyzed the correlation between SNHG1, miR-454 and zinc finger E-box-binding homeobox 1 (ZEB1) using a dual-luciferase reporter assay. Alterations in cell metastasis and invasiveness were observed using wound-healing and Transwell invasion assays, respectively. Tumor xenografts allowed us to monitor liver metastasis of mice injected with A2780 cells. We found that SNHG1 is overexpressed in OC. Downregulation of SNHG1 promoted miR-454 expression and reduced ZEB1 levels. In addition, knockdown of SNHG1, also reduced the aggressiveness of A2780 and SK-OV3 cells. Furthermore, SNHG1 downregulation by siRNA hindered cell migration and invasion; however, this effect was reversed by co-transfection of miR-454 into A2780 and SK-OV3 cells. Moreover, SNHG1 increased ZEB1 expression by downregulating miR-454 and activated Akt signaling, thereby promoting epithelial-mesenchymal transition and enhancing the invasiveness of OC cells. Tumor xenograft analyses confirmed that SNHG1 affects OC proliferation and metastasis in vivo. In summary, our data demonstrate that SNHG1 plays crucial roles in tumor progression and may be a useful maker for OC prognosis.

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The role of the long non‐coding RNA TDRG1 in epithelial ovarian carcinoma tumorigenesis and progression through miR‐93/RhoC pathway

Cited by 21 publications

References 26 publications

LncRNA TDRG1/miR‐214‐5p axis affects preeclampsia by modulating trophoblast cells

LncRNA TDRG1/miR‐214‐5p axis affects preeclampsia by modulating trophoblast cells

The lncRNA TDRG1 promotes cell proliferation, migration and invasion by targeting miR-326 to regulate MAPK1 expression in cervical cancer

Long non‐coding RNA SNHG1 stimulates ovarian cancer progression by modulating expression of miR‐454 and ZEB1

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