MiR-203 controls proliferation, migration and invasive potential of prostate cancer cell lines

Viticchié, Giuditta; Lena, Anna Maria; Latina, A; Formosa, Amanda; Gregersen, Lea H.; Lund, Anders H.; Bernardini, Sergio; Mauriello, Alessandro; Miano, Roberto; Spagnoli, Luigi Giusto; Knight, Richard; Candi, Eleanora; Melino, Gerry

doi:10.4161/cc.10.7.15180

Cited by 186 publications

(154 citation statements)

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“…Collectively, our findings support the idea that miR-203 may be a mediator of the p53-Puma pathway. In addition, we demonstrated that overexpressed miR-203 improved gemcitabine sensitivity; a finding consistent with other data which showed that miR-203 inhibits cell proliferation and invasiveness in prostate carcinoma, and induces apoptosis in transitional cell carcinom (38). Moreover, Feber et al revealed that miR-203 suppresses cell proliferation in esophageal carcinoma (22), while Miao et al showed that miR-203 inhibits cell migration, invasion, and the epithelial-mesenchymal transition (EMT) via caveolin-1 in pancreatic carcinoma (39).…”

Section: Overexpressed Mir-203 Induces Apoptosis and Decreases Cell Isupporting

confidence: 80%

MicroRNA-203 induces apoptosis by upregulating Puma expression in colon and lung cancer cells

Funamizu

Lacy

Kamada

et al. 2015

International Journal of Oncology

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Abstract. The present study investigated the relationship between and the p53 upregulated modulator of apoptosis (Puma) in colon (HCT116) and lung cancer (A549) cells. Colon and lung cancer cell lines were selected for this study since a relationship between p53/miR-203 and p53/Puma has been established in both cancers. In the present study, adriamycin and nutlin-3 were used to activate p53, which induced both miR-203 and Puma expression in HCT116 cells. In contrast, HCT 116 cells with downregulated p53 showed decreased miR-203 and Puma expression. Importantly, we found that overexpressed miR-203 in HCT116 cells resulted in significantly increased Puma expression (P<0.05). Based on these findings, we hypothesized that another limb of the p53/Puma axis depends on miR-203 expression. To further validate this relationship, we used lung cancer cells (A549) and found that activated p53 increased both miR-203 and Puma expression. In addition, we found that Puma expression remained elevated in cells with overexpressed miR-203 in the presence of p53 downregulation. Cumulatively, our data purport that p53 not only increased Puma expression directly, but that it may also do so through miR-203. Additionally, functional studies revealed that miR-203 overexpression induced apoptosis and inhibited cell invasiveness.

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Section: Overexpressed Mir-203 Induces Apoptosis and Decreases Cell Isupporting

confidence: 80%

MicroRNA-203 induces apoptosis by upregulating Puma expression in colon and lung cancer cells

Funamizu

Lacy

Kamada

et al. 2015

International Journal of Oncology

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“…We previously showed that miR-203 inhibited EMT by targeting mesenchymal marker Snail in ovarian cancer cells (19). Interestingly, ASAP1 was identified as a target gene of miR-203 and overexpression of miR-203 led to inhibition of EMT in prostate cancer cells (20). Although we did not test whether miR-203 directly regulated ASAP1 and thereby inhibited EMT in ovarian cancer cells, it was highly possible that ASAP1 mediated EMT was also regulated by miR-203 in ovarian cancer cells.…”

Section: Discussionmentioning

confidence: 95%

Lentiviral vector mediated-ASAP1 expression promotes epithelial to mesenchymal transition in ovarian cancer cells

et al. 2018

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Abstract. Ovarian cancer is one of the most common malignancies in women and has a high mortality rate due to metastatic progression and tumor recurrence. ASAP1 (ArfGAP with SH3 Domain, Ankyrin Repeat and PH Domain 1) is an ADP-ribosylation factor GTPase-activating protein, which is involved in tumor metastasis. However, the role of ASAP1 in ovarian cancer is completely unknown. The present study reported that ASAP1 was highly expressed in ovarian carcinoma, and expression positively-correlated with overall poor survival and prognosis of patients. Lentiviral vector mediated ASAP1 expression promoted cell migration and invasion in ovarian cancer cell lines SKOV3 and OVCAR3. In addition, ASAP1 promoted cell proliferation, survival and inhibited chemotherapy drug paclitaxel-induced cell apoptosis. Furthermore, ASAP1 expression promoted epithelial to mesenchymal transition (EMT) by upregulating the mesenchymal cell markers N-cadherin and vimentin, and downregulating epithelial cell marker E-cadherin in the ovarian cancer cell lines. The data indicate for the first time that ASAP1 exhibits an oncogenic role by promoting EMT in ovarian cancer cells. IntroductionOvarian cancer is one of the most common gynecological malignancies with a high mortality rate (1). In 2017, 22,440 new cases and 14,080 deaths of ovarian cancer were estimated to occur in the United States (2). At the time of diagnosis, the majority of ovarian cancer patients have already progressed to advanced disease, due to the lack of early clinical symptoms, which results in high mortality (3). However, the molecular mechanisms underlying the tumor metastasis and chemoresistance in ovarian cancer are not well understood. The epithelial-mesenchymal transition (EMT) contributes to the tumor metastasis and chemoresistance (4). EMT is a biological process accompanied by the loss of cell adherence junctions and apical-basal polarity, and acquisition of the mesenchymal phenotype to increase cell motility and invasiveness (5). EMT marker gene expression is altered during the EMT process with downregulation of epithelial markers such as E-cadherin and upregulation of mesenchymal markers, including Snai1 and 2, N-cadherin, vimentin, Zeb 1/2, and Twist1/2 (6,7). ASAP1 (ArfGAP with SH3 Domain, Ankyrin Repeat and PH Domain 1) protein has N-terminal BAR, PH, ARF GAP, ankyrin repeat, proline-rich, and C-terminal SH3 domains (8). ASAP1 expression is upregulated in a variety of cancers as compared to normal tissue, and correlates with poor survival and prognosis in colorectal, and neck and head cancer patients (9,10). In breast cancer ASAP1expression contributes to tumor invasion and metastasis (11). ASAP1 is upregulated in ovarian cancer and associated with poor patient survival and prognosis (12). However, the function of ASAP1 in ovarian cancer has not been investigated.In the present study, we investigated the role of ASAP1 in ovarian cancer cells using lentiviral vector mediated overexpression. We demonstrated that ASAP1 was highly expressed in ovarian cancer and as...

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“…In the recent study, miR-203 has significantly low expression in cancer tissues compared to non-tumor counterparts (Viticchiè et al, 2011;Takeshita et al, 2012;Gu et al, 2013), while there were up-regulation of miR-203 was observed in pancreatic adenocarcinomas and breast, cancers (Naoki et al, 2010;Madhavan et al, 2012), we think the differential expression of miRNAs may be the result of tissue-specific differences. Just as Baffa et al suggested (Baffa et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Aberrant Expression of miR-20a and miR-203 in Cervical Cancer

Song¹,

Yao²,

Chen³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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MiR-203 controls proliferation, migration and invasive potential of prostate cancer cell lines

Cited by 186 publications

References 0 publications

MicroRNA-203 induces apoptosis by upregulating Puma expression in colon and lung cancer cells

MicroRNA-203 induces apoptosis by upregulating Puma expression in colon and lung cancer cells

Lentiviral vector mediated-ASAP1 expression promotes epithelial to mesenchymal transition in ovarian cancer cells

Aberrant Expression of miR-20a and miR-203 in Cervical Cancer

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