Expression of Plectin-1 and Trichohyalin in Human Tongue Cancer Cells

Tamura, Isao; Ueda, Katsura; Nishikawa, Tetsunari; Kamada, Aiko; Okamura, Tomoharu; Matsuda, Yoshihisa; Ueno, K.; Yoshikawa, Yusuke; Domae, Eisuke; Tominaga, Kazuhiro; Kumabe, Shunji; Ikeo, Takashi; Tanaka, Akio

doi:10.4236/ojst.2018.86019

Cited by 3 publications

(3 citation statements)

References 25 publications

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“…In osteoclasts, plectin acts as a scaffold for the recruitment of Src and Pyk2 [20] substrates. Plectin is a candidate biomarker for certain types of tumors because its expression in tumor specimens is higher than that in surrounding normal tissues [21][22][23]. Recently, a novel anti-tumor agent targeting plectin, ruthenium pyridinecarbothioamide, was shown to suppress tumor growth in a B16 melanoma cell model [24,25].…”

Section: Introductionmentioning

confidence: 99%

Plectin promotes melanoma tumor formation by regulation of Rous sarcoma oncogene activity

Mizuta

Matsubara

Goto

et al. 2022

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Background Melanoma is a malignant tumor that is characterized by high proliferation and aggressive metastasis. To address the efficient treatment of melanoma, the molecular mechanisms of the proto-oncogene, Rous sarcoma oncogene (Src), which is highly activated and promotes cell proliferation, migration, adhesion, and metastasis in melanoma, should be understood. Plectin has recently been identified as an Src-binding protein that regulates Src activity in osteoclasts. Plectin, a cytoskeleton-regulatory protein, is a candidate biomarker of certain tumors because of its high expression and the target of anti-tumor reagents such as ruthenium pyridinecarbothioamide, although the molecular mechanisms by which plectin works in melanoma are still unclear. In this study, we examined its pathological role in melanoma tumor formation. Methods We established plectin knock-out B16 cells, the mouse melanoma cell line, with CRISPR/Cas9 system. The expression of plectin and activity of Src were examined by western blotting analysis. The tumors were formed at 2 weeks after subcutaneous injection of B16 cells in nude mice and analyzed by Hematoxylin-Eosin (H-E) staining. Cell proliferation was evaluated by cell counting kit-8, expression of cyclin D1 and Ki-67. Cell aggregation and adhesion were assessed by spheroid formation and cell adhesion assay.Results Depletion of plectin induced low-density and sparce tumor formation by melanoma cells in vivo. In vitro experiments revealed that plectin-deficient melanomas exhibit reduced cell proliferation and suppressed cell-to-cell adhesion. Because Src activity is reduced in plectin-deficient melanomas, we examined the relationship between plectin and Src signaling. Src overexpression restored Src activity and rescued cell proliferation and cell-to-cell adhesion in plectin-deficient melanomas. Conclusion: These results suggest that plectin is required for tumor formation by promoting cell proliferation and cell-to-cell adhesion through Src signaling activity in melanoma cells.

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Section: Introductionmentioning

confidence: 99%

Plectin promotes melanoma tumor formation by regulation of Rous sarcoma oncogene activity

Mizuta

Matsubara

Goto

et al. 2022

Preprint

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“…In osteoclasts, plectin acts as a scaffold for recruitment of Src and the Pyk2 19 substrate. Plectin is a candidate biomarker for certain types of cancers because plectin expression in tumor specimens is higher than surrounding normal tissues [20][21][22] . Recently, a novel anticancer agent targeting plectin, ruthenium pyridinecarbothioamide, was shown to suppress tumor growth in a B16 melanoma cell model 23,24 .…”

Section: Introductionmentioning

confidence: 99%

Plectin Promotes Melanoma Tumor Formation by Regulation of Src Activity

Mizuta

Matsubara

Goto

et al. 2021

Preprint

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Melanoma is malignant cancer characterized by high proliferation and aggressive metastasis. To address efficient treatment for melanoma, we should understand the molecular mechanisms for a proto-oncogene Src, which is highly activated and promotes cell proliferation, migration, adhesion, and metastasis in melanoma. We recently identified plectin as the Src binding protein and regulates Src activity in osteoclasts. Plectin, a cytoskeleton regulatory protein, is focused as the candidates of biomarker of certain tumors because of higher expression and the candidate of anti-tumor reagents such as ruthenium pyridinecarbothioamide although the molecular mechanisms how plectin works in melanoma is unclear. In this study, we examined the pathological role in melanoma tumor formation. Depletion of plectin induced low density and sparce tumor formation by melanoma cells in vivo. In vitro experiment revealed that plectin deficient melanomas reduced cell proliferation and suppressed cell-to-cell adhesion. Because Src activity was reduced in plectin deficient melanomas, we examined the relationship between plectin and Src signaling. Src overexpression that restored Src activity rescued cell proliferation and cell-to-cell adhesion of plectin deficient melanomas. These results suggest that plectin is required for tumor formation by promoting cell proliferation and cell-to-cell adhesion via Src signaling activity in melanoma.

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“…In osteoclasts, plectin acts as a scaffold for the recruitment of Src and Pyk2 substrates [22]. Plectin is a candidate biomarker for certain types of tumors because its expression in tumor specimens is higher than that in surrounding normal tissues [23][24][25]. Recently, a novel anti-tumor agent targeting plectin, ruthenium pyridinecarbothioamide, was shown to suppress tumor growth in a B16 melanoma cell model [26,27].…”

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confidence: 99%

Plectin promotes tumor formation by B16 mouse melanoma cells via regulation of Rous sarcoma oncogene activity

et al. 2022

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Background Melanoma is a malignant tumor characterized by high proliferation and aggressive metastasis. To address the molecular mechanisms of the proto-oncogene, Rous sarcoma oncogene (Src), which is highly activated and promotes cell proliferation, migration, adhesion, and metastasis in melanoma. Plectin, a cytoskeletal protein, has recently been identified as a Src-binding protein that regulates Src activity in osteoclasts. Plectin is a candidate biomarker of certain tumors because of its high expression and the target of anti-tumor reagents such as ruthenium pyridinecarbothioamide. The molecular mechanisms by which plectin affects melanoma is still unclear. In this study, we examined the role of plectin in melanoma tumor formation. Methods We used CRISPR/Cas9 gene editing to knock-out plectin in B16 mouse melanoma cells. Protein levels of plectin and Src activity were examined by western blotting analysis. In vivo tumor formation was assessed by subcutaneous injection of B16 cells into nude mice and histological analysis performed after 2 weeks by Hematoxylin-Eosin (H&E) staining. Cell proliferation was evaluated by direct cell count, cell counting kit-8 assays, cyclin D1 mRNA expression and Ki-67 immunostaining. Cell aggregation and adhesion were examined by spheroid formation, dispase-based dissociation assay and cell adhesion assays. Results In in vivo tumor formation assays, depletion of plectin resulted in low-density tumors with large intercellular spaces. In vitro experiments revealed that plectin-deficient B16 cells exhibit reduced cell proliferation and reduced cell-to-cell adhesion. Since Src activity is reduced in plectin-deficient melanomas, we examined the relationship between plectin and Src signaling. Src overexpression in plectin knockout B16 cells rescued cell proliferation and improved cell-to-cell adhesion and cell to extracellular matrix adhesion. Conclusion These results suggest that plectin plays critical roles in tumor formation by promoting cell proliferation and cell-to-cell adhesion through Src signaling activity in melanoma cells.

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Expression of Plectin-1 and Trichohyalin in Human Tongue Cancer Cells

Cited by 3 publications

References 25 publications

Plectin promotes melanoma tumor formation by regulation of Rous sarcoma oncogene activity

Plectin promotes melanoma tumor formation by regulation of Rous sarcoma oncogene activity

Plectin Promotes Melanoma Tumor Formation by Regulation of Src Activity

Plectin promotes tumor formation by B16 mouse melanoma cells via regulation of Rous sarcoma oncogene activity

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