Protein Kinase C: A Putative New Target for the Control of Human Medullary Thyroid Carcinoma Cell Proliferation in Vitro

Molè, Daniela; Gentilin, Erica; Gagliano, Teresa; Tagliati, Federico; Bondanelli, Marta; Pelizzo, Maria Rosa; Rossi, Martina; Filieri, Carlo; Pansini, Giancarlo; Uberti, Ettore C. degli; Zatelli, Maria Chiara

doi:10.1210/en.2011-1988

Cited by 16 publications

(12 citation statements)

References 43 publications

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“…The upregulation or downregulation of PKC and their isoenzyme or their biological effect had previously been studied in human tumor samples (13)(14)(15)(16)(17). Downregulation of PKC isozymes was associated with the occurrence and progression of several human cancer types.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of PKCα reduces the ability of migration of kidney cancer cells but has no impact on cell apoptosis

Zhan

Kong

Zhang

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Kidney cancer is among the most important causes of cancer-associated mortality worldwide. The present study aimed to evaluate protein kinase C α (PKCα) expression in kidney cancer tissues and cell lines, and its significance in apoptosis and migration. Expression of PKCα was analyzed using quantitative polymerase chain reaction and western blotting. In addition, the inhibitor of PKCα (calphostin C and GO6976) was used to treat kidney cancer cells. The ACHN cell line was generated with PKCα-small-interfering RNA (siRNA) and a stable expression of PKCα, in order to facilitate the analysis of apoptosis and migration of PKCα during knockdown and inactivation. Flow cytometry was used to determine the rates of apoptosis. Immunohistochemical staining was used to identify the localization of PKCα in renal clear cell carcinoma and normal sections. PKCα expression in normal tissues was found to be greater than in cancerous tissues. Furthermore, apoptosis was not promoted with PKCα inhibitors or PKCα-siRNA treatment, and a decrease of the migration ability was observed following transfection with PKCα-dominant negative. The results indicated that inhibition of PKCα might not contribute to apoptosis progression in kidney carcinoma.

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Section: Discussionmentioning

confidence: 99%

Inhibition of PKCα reduces the ability of migration of kidney cancer cells but has no impact on cell apoptosis

Zhan

Kong

Zhang

et al. 2017

Experimental and Therapeutic Medicine

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“…The role of PKC has previously been studied in relation to thyroid tumourigenesis and thyroid cancer (Hoelting et al 1997, Knauf et al 2002, Mole et al 2012. In FTC-133 cells, PKC activation by PMA increased cell invasion (Hoelting et al 1997).…”

Section: Discussionmentioning

confidence: 99%

The impact of CLAUDIN-1 on follicular thyroid carcinoma aggressiveness

Zwanziger¹,

Badziong²,

Ting³

et al. 2015

Endocrine-Related Cancer

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CLAUDIN-1 belongs to the family of transmembrane tight junction proteins tightening the paracellular cleft of epithelial cells. In human malignancies, CLAUDIN-1 is often dysregulated and located in subcellular compartments, particularly in the nucleus where it may influence cellular behaviour. Here, we studied CLAUDIN-1 in relation to the biological characteristics of follicular thyroid carcinoma (FTC). CLAUDIN-1 immuno-staining showed loss of membrane expression and increased nuclear CLAUDIN-1 localization in FTC metastases. CLAUDIN-1 function was further investigated in two different follicular thyroid carcinoma cell lines: FTC-133 isolated from a regional lymph node metastasis and FTC-238 derived from a lung metastasis. In both cell lines CLAUDIN-1 expression was demonstrated in the cell nuclei with a significantly higher protein expression in FTC-238 compared to FTC-133 cells. Interestingly, in vitro scratch assay revealed enriched nuclear CLAUDIN-1 expression near the scratch. Furthermore, the increase of the pathogenic character of FTC-133 cells by RASV12 transfection was associated with elevated CLAUDIN-1 expression and enhanced cell migration, invasion and proliferation. Likewise over-expression of nuclear CLAUDIN-1 in FTC-133 cells resulted in increased cell migration and invasion. Conversely, CLAUDIN-1 downregulation in FTC-238 cells by siRNA resulted in decreased cell migration and invasion and was accompanied by reduced phosphoPKC expression. Moreover, activation and inhibition of PKC resulted in CLAUDIN-1 up-and downregulation in FTC cells respectively. These data suggest an impact of CLAUDIN-1 on follicular thyroid carcinoma aggressiveness, which could potentially be influenced by PKC activity.

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“…Furthermore, PKC II inhibition by enzastaurin leads to the reduction of medullary thyroid carcinoma cell proliferation and survival, indicating that PKC II is required in these processes [496].…”

Section: Thyroidmentioning

confidence: 99%

Protein Kinase C (PKC) Isozymes and Cancer

Kang

2014

New Journal of Science

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Protein kinase C (PKC) is a family of phospholipid-dependent serine/threonine kinases, which can be further classified into three PKC isozymes subfamilies: conventional or classic, novel or nonclassic, and atypical. PKC isozymes are known to be involved in cell proliferation, survival, invasion, migration, apoptosis, angiogenesis, and drug resistance. Because of their key roles in cell signaling, PKC isozymes also have the potential to be promising therapeutic targets for several diseases, such as cardiovascular diseases, immune and inflammatory diseases, neurological diseases, metabolic disorders, and multiple types of cancer. This review primarily focuses on the activation, mechanism, and function of PKC isozymes during cancer development and progression.

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Protein Kinase C: A Putative New Target for the Control of Human Medullary Thyroid Carcinoma Cell Proliferation in Vitro

Cited by 16 publications

References 43 publications

Inhibition of PKCα reduces the ability of migration of kidney cancer cells but has no impact on cell apoptosis

Inhibition of PKCα reduces the ability of migration of kidney cancer cells but has no impact on cell apoptosis

The impact of CLAUDIN-1 on follicular thyroid carcinoma aggressiveness

Protein Kinase C (PKC) Isozymes and Cancer

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