In colon carcinogenesis, the cytoskeletal protein gelsolin is down-regulated during the transition from adenoma to carcinoma

Gay, Frédérick; Estornes, Yann; Saurin, Jean‐Christophe; Joly-Pharaboz, Marie-Odile; Friederich, Evelyne; Scoazec, Jean‐Yves; Abello, Jacques

doi:10.1016/j.humpath.2008.02.020

Cited by 32 publications

(39 citation statements)

References 32 publications

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“…Reduced gelsolin expression level has been described for many cancer tissues including breast, colon, prostate, ovary and bladder (Dong et al, 2002;Gay et al, 2008;Furuuchi et al, 1997;Lee et al, 1999;Noske et al, 2005;Tanaka et al, 1995;Winston et al, 2001). However a number of studies suggested that elevated gelsolin expression was significantly associated with poor prognosis of patient survival (Shieh et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

“…However the exact role of gelsolin in carcinogenesis is still controversial (Cunningham et al, 1991;Li et al, 2010). Gelsolin down-regulation has been described for tumor cells isolated from breast (Dong et al, 2002;Winston et al, 2001), colon (Furuuchi et al, 1997;Gay et al, 2008), ovarium (Noske et al, 2005), prostate (Lee et al, 1999) and bladder cancer (Tanaka et al, 1995). On the contrary, a number of studies have reported that upregulation of gelsolin is associated with poor prognosis and higher risk of cancer recurrence.…”

Section: Introductionmentioning

confidence: 99%

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Gelsolin affects the migratory ability of human colon adenocarcinoma and melanoma cells

et al. 2012

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Gelsolin affects the migratory ability of human colon adenocarcinoma and melanoma cells

et al. 2012

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“…Several reports showed that gelsolin expression was low in the poorly differentiated stages of bladder cancer, 24 ovarian cancer, 25 and colon cancer. 26 Lee et al 27 examined gelsolin expression in 72 prostatectomy specimens with adenocarcinoma and 8 nonneoplastic prostates from autopsies. The expression was decreased in prostatic adenocarcinoma in comparison with nonproliferative tissue.…”

Section: Gelsolin-mediated Invasion Of Prostate Cancer K Hashimoto Et Almentioning

confidence: 99%

The potential of neurotensin secreted from neuroendocrine tumor cells to promote gelsolin-mediated invasiveness of prostate adenocarcinoma cells

Hashimoto

Kyoda

Tanaka

et al. 2015

Laboratory Investigation

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Neuroendocrine (NE) cells in prostate cancer have been shown to be associated with the progression of prostate cancer. However, little is known about the molecular basis of this association. We have previously demonstrated that NE cells promote metastasis of a human prostate cancer cell line (LNCaP) with overexpression of the gelsolin gene. The purpose of this study was to investigate the interactions between NE cells and LNCaP cells and the involvement of gelsolin in contributing to the invasive potential of LNCaP cells. In addition, we examined whether neurotensin induced gelsolin-mediated invasion. We used the NE cell line NE-CS that was established from the prostate of the LPB-Tag 12T-10 transgenic mouse. Small interfering RNA (siRNA) targeting gelsolin or not targeting it was transfected into LNCaP cells.

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“…For example, high GSN expression in oral cancers is related to a poor clinical outcome for patients with metastasis [21]. In contrast, GSN expression is frequently down-regulated in ovarian, stomach and colon cancers [22,23,24]. In our study, the up-regulation of GSN expression may play a role in inhibiting the metastasis of SPC-A-1sci cells transfected with miR-193a-3p.…”

Section: Discussionmentioning

confidence: 61%

Quantitative Proteomic Analysis of the Metastasis-Inhibitory Mechanism of miR-193a-3p in Non-Small Cell Lung Cancer

Deng

Yan

et al. 2015

Cell Physiol Biochem

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Background: microRNAs can repress the expression of target genes by destabilizing their mRNAs or by inhibiting their translation. Our previous findings suggested that miR-193a-3p inhibited the progression of NSCLC both in vitro and in vivo. However, the biological processes and molecular pathways through which this miRNA exerts its positive effects are unknown. Methods: To explore the molecular mechanisms by which miR-193a-3p inhibited NSCLC metastasis, we investigated the changes in the protein profile of SPC-A-1sci (highly metastatic) cells in response to the up-regulation of miR-193a-3p expression using a proteomics approach (iTRAQ combined with NanoLC-MS/MS). Changes in the profiles of the expressed proteins were verified using western blotting and were analyzed using the DAVID and STRING programs. Results: In the two replicated experiments, 4962/4946 proteins were identified, and the levels of expression of 4923/4902 proteins were quantified. In total, 112 of these proteins were differentially expressed. Among them, the up-regulated levels of expression of two of the 62 proteins with up-regulated expression (PPP2R2A and GSN) and the down-regulated levels of expression four of the 50 proteins with down-regulated expression (LMNB2, UHRF1, G3BP1, and HNRNPU) were verified using western blotting. The bioinformatics analysis revealed the interactions and signaling networks of these differentially expressed proteins. Conclusion: miR-193a-3p inhibited the metastasis of lung cancer cells by deregulating the expression of tumor-related proteins. These findings may improve the understanding of the molecular mechanisms underlying the metastatic-inhibitory effect of miR-193a-3p on lung cancer cells.

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In colon carcinogenesis, the cytoskeletal protein gelsolin is down-regulated during the transition from adenoma to carcinoma

Cited by 32 publications

References 32 publications

Gelsolin affects the migratory ability of human colon adenocarcinoma and melanoma cells

Gelsolin affects the migratory ability of human colon adenocarcinoma and melanoma cells

The potential of neurotensin secreted from neuroendocrine tumor cells to promote gelsolin-mediated invasiveness of prostate adenocarcinoma cells

Quantitative Proteomic Analysis of the Metastasis-Inhibitory Mechanism of miR-193a-3p in Non-Small Cell Lung Cancer

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