Non-canonical signaling pathway of SNAI2 induces EMT in ovarian cancer cells by suppressing miR-222-3p transcription and upregulating PDCD10

Fan, Lili; Han, Lei; Zhang, Sai; Peng, Yuan; Fu, Chunyan; Shu, Guang; Yin, Gang

doi:10.7150/thno.43198

Cited by 61 publications

(68 citation statements)

References 48 publications

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“…Moreover, a recent work from Fan L. et al. demonstrated that SNAI2 enhances ovarian cancer cells migration through the axis miR-222-3/PDCD10 [7] . All together our results identifies PDCD10 as an important player in cancer development and a promising therapeutic target.…”

Section: Discussionmentioning

confidence: 99%

“…In fact, whereas PDCD10 has been shown to be up-regulated in oral, colorectal and pancreatic cancer [34] , [35] , [36] , the loss of PDCD10 has been associated to the progression of glioblastoma [37] . PDCD10 has been shown to be the target for the tumor suppressor activity of miR-222-3p in ovarian cancer [7] , of miR-103 in prostate or lung cancer [ 38 , 39 ] and of miR-26a-5p and of miR-26b-5p in bladder cancer [40] . On the other hand, mir-425-5p-induced up-regulation of PDCD10 promotes chemo-resistance in colorectal cancer cells [41] .…”

Section: Discussionmentioning

confidence: 99%

“…All together our results identifies PDCD10 as an important player in cancer development and a promising therapeutic target. In consideration of the relevant role of microRNAs in PDCD10 regulation [ 7 , [38] , [39] , [40] ], a promising therapeutic option is represented by microRNAs such as miR-222-3p, miR103 and miR-26a/b-5p targeting PDCD10. Other therapeutic candidates are represented by ERK inhibitors, especially for their potential in overcoming resistance towards drugs targeting upstream molecules [50] .…”

Section: Discussionmentioning

confidence: 99%

“…PDCD10, also known as CCM3, belongs to the CCM family of proteins and was first identified as one of the genes responsible for Cerebral Cavernous Malformations [5] . Subsequently, it was shown to promote assembly of the Golgi complex, cell proliferation and migration [ 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

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Genome-wide analysis of copy number alterations led to the characterisation of PDCD10 as oncogene in ovarian cancer

Marco

Zoppoli

Rinaldo

et al. 2021

Translational Oncology

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Highlights We have identified 201 altered chromosomal bands and 3300 altered genes in human ovarian cancer samples. The gene encoding for PDCD10 was selected for further studies. PDCD10 was found to be over-expressed in primary cancer samples and in the corresponding metastatic lesions. High PDCD10 expression correlates with grade, nodal involvement or advanced FIGO stage. PDCD10 is involved in the control of cell growth and motility in vitro as well as tumorigenicity in vivo .

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Genome-wide analysis of copy number alterations led to the characterisation of PDCD10 as oncogene in ovarian cancer

Marco

Zoppoli

Rinaldo

et al. 2021

Translational Oncology

View full text Add to dashboard Cite

show abstract

“…Many miRNAs regulate tumor invasion and metastasis through EMT-related mechanisms. In ovarian cancer, the EMT-inducing factor SNAI2 up-regulates PDCD10 by inhibiting miR-222-3p to induce EMT [33]. MiR-186 overexpression in ovarian cancer cells reduces Twist1 expression, thus making the cells highly sensitive to cisplatin in vitro and in vivo [34].…”

Section: Discussionmentioning

confidence: 99%

RAC1/miR-3613/RAC1 feedback loop contributes to ovarian cancer progression

Leng

Meng

et al. 2021

Preprint

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The RAC1 signal pathway is involved in various tumor cell biological processes. Here, the role of RAC1-miR-3613-RAC1 negative feedback loop in ovarian cancer was explored. Results showed that RAC1 knockdown up-regulated miR-3613, which in turn inhibited RAC1 expression. RAC1 counteracted the inhibitory effect of miR-3613 on the proliferation and invasion of ovarian cancer cells in vitro and on the tumor growth in vivo. In ovarian cancer, miR-3613 expression was negatively correlated with RAC1, and patients with low miR-3613 expression had poor prognosis. These findings indicate the role of RAC1-miR-3613-RAC1 negative feedback loop in the malignant progression of ovarian cancer and its possible therapeutic values.

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PDCD10promotes proliferation, migration, and invasion of osteosarcoma by inhibiting apoptosis and activatingEMTpathway

Fei

Huo

et al. 2022

Cancer Medicine

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Background Osteosarcoma, a common primary malignant tumor, occurs in children and adolescents with a poor prognosis. The current treatment methods are various, while the five‐year survival rate of patients has not been significantly improved. As a member of the programmed death factor (PDCD) family, programmed death factor 10 (PDCD10) plays a role in regulating cell apoptosis. Several studies of PDCD10 in CCM and cancers have been reported before. However, there are no relevant research reports on the effects of PDCD10 on osteosarcoma. Methods We used bioinformatics analysis, IHC, and clinical data to confirm the expression of PDCD10 and its correlation with prognosis in osteosarcoma. Then, we used shRNAs and cDNA to knock down or overexpress PDCD10 in U2OS and MG63 cell lines. A series of function assays such as CCK8, Wound healing test, Plate cloning formation assay, and Transwell were done to confirm how PDCD10 affects osteosarcoma. Animal assays were done to confirm the conclusions in cell lines. At last, WB was used to measure the protein expression levels of apoptosis and the EMT pathway. Results PDCD10 was highly expressed in patients with osteosarcoma and correlated with prognosis; PDCD10 knockdown inhibited osteosarcoma growth, proliferation, migration, and invasion; PDCD10 overexpression promoted osteosarcoma growth, proliferation, migration, and invasion. In vivo experiments confirmed the conclusions in cell lines; PDCD10 inhibited apoptosis and activated the EMT pathway. Conclusions In this study, it was found that PDCD10 was highly expressed in patients with osteosarcoma, and it was closely related to patient prognosis. PDCD10 inhibited tumor cell apoptosis and promoted tumor progression by activating the EMT pathway. These findings may provide a potential target for gene therapy of osteosarcoma.

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Non-canonical signaling pathway of SNAI2 induces EMT in ovarian cancer cells by suppressing miR-222-3p transcription and upregulating PDCD10

Cited by 61 publications

References 48 publications

Genome-wide analysis of copy number alterations led to the characterisation of PDCD10 as oncogene in ovarian cancer

Genome-wide analysis of copy number alterations led to the characterisation of PDCD10 as oncogene in ovarian cancer

RAC1/miR-3613/RAC1 feedback loop contributes to ovarian cancer progression

PDCD10promotes proliferation, migration, and invasion of osteosarcoma by inhibiting apoptosis and activatingEMTpathway

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