Increased expression of T‐plastin gene in cisplatin‐resistant human cancer cells: identification by mRNA differential display

Hisano, Terumasa; Ono, Masahiro; Nakayama, Masaharu; Naito, Seiji; Kuwano, Michihiko; Wada, Morimasa

doi:10.1016/s0014-5793(96)01150-7

Cited by 44 publications

(35 citation statements)

References 37 publications

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“…The PLS3 gene, located on chromosome Xq23, functions to polymerize actin fibers through inhibition of cofilin-mediated actin depolymerization (38). It is known that cisplatin-or UV-resistant cancer cell lines overexpress PLS3 (39,40), and CRC lines overexpressing PLS3 acquire invasiveness through downregulation of Ecadherin (41). Moreover, the GSEA (public database) results provided supportive evidence that PLS3 might be involved in EMT via TGFb-1 stimulation and that PLS3 was related to CRC metastasis and cancer stemness as well.…”

Section: Discussionmentioning

confidence: 99%

Plastin3 Is a Novel Marker for Circulating Tumor Cells Undergoing the Epithelial–Mesenchymal Transition and Is Associated with Colorectal Cancer Prognosis

et al. 2013

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Circulating tumor cells (CTC) in blood have attracted attention both as potential seeds for metastasis and as biomarkers. However, most CTC detection systems might miss epithelial-mesenchymal transition (EMT)-induced metastatic cells because detection is based on epithelial markers. First, to discover novel markers capable of detecting CTCs in which EMT has not been repressed, microarray analysis of 132 colorectal cancers (CRC) from Japanese patients was conducted, and 2,969 genes were detected that were overexpressed relative to normal colon mucosa. From the detected genes, we selected those that were overexpressed CRC with distant metastasis. Then, we analyzed the CRC metastasis-specific genes (n ¼ 22) to determine whether they were expressed in normal circulation. As a result, PLS3 was discovered as a CTC marker that was expressed in metastatic CRC cells but not in normal circulation. Using fluorescent immunocytochemistry, we validated that PLS3 was expressed in EMTinduced CTC in peripheral blood from patients with CRC with distant metastasis. PLS3-expressing cells were detected in the peripheral blood of approximately one-third of an independent set of 711 Japanese patients with CRC. Multivariate analysis showed that PLS3-positive CTC was independently associated with prognosis in the training set (n ¼ 381) and the validation set [n ¼ 330; HR ¼ 2.17; 95% confidence interval (CI) ¼ 1.38-3.40 and HR ¼ 3.92; 95% CI ¼ 2.27-6.85]. The association between PLS3-positive CTC and prognosis was particularly strong in patients with Dukes B (HR ¼ 4.07; 95% CI ¼ 1.50-11.57) and Dukes C (HR ¼ 2.57; 95% CI ¼ 1.42-4.63). PLS3 is a novel marker for metastatic CRC cells, and it possesses significant prognostic value. Cancer Res; 73(7); 2059-69. Ó2012 AACR.

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Section: Discussionmentioning

confidence: 99%

Plastin3 Is a Novel Marker for Circulating Tumor Cells Undergoing the Epithelial–Mesenchymal Transition and Is Associated with Colorectal Cancer Prognosis

et al. 2013

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“…Both T-Plastin and Caldesmon are actin bundling proteins, and expression of such cytoskeletal proteins have been widely reported to be correlated with oncogenic phenotypes (Green et al, 1990;Davies et al, 1993;De Silva et al, 1994). Tplastin, one of three plastin isoforms, is upregulated up to 12-fold in cisplatin-resistant tumor cells by comparison to their parental non-resistant cells, and the expression of antisense T-plastin RNA restores cisplatin sensitivity (Hisano et al, 1996). Caldesmon confers morphological changes on ®broblasts when overexpressed (Surgucheva and Bryan, 1995).…”

Section: Discussionmentioning

confidence: 99%

EB-1, a tyrosine kinase signal transduction gene, is transcriptionally activated in the t(1;19) subset of pre-B ALL, which express oncoprotein E2a-Pbx1

McGrath

Pasillas

et al. 1999

Oncogene

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“…3 Interestingly, by differential display analysis, the expression level of T-plastin has also been shown to correlate with cellular resistance to DNA-damaging agents. 37,38 CM3 was identified as SAP18, a component of a nuclear complex involved in transcription repression by means of histone deacetylation. 26 LV2 appeared to be the mitochondrial "mechano-enzyme" HMP, 23 also known as mitofilin.…”

Section: Differential Display Analysis Of Immunoselected Ma-11 Cell Pmentioning

confidence: 99%

Differential display analysis of breast carcinoma cells enriched by immunomagnetic target cell selection: Gene expression profiles in bone marrow target cells

Ree

Engebraaten

Hovig

et al. 2001

Intl Journal of Cancer

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The red bone marrow (BM) is an important indicator organ of hematogenous micrometastatic spread of carcinomas. Characterization of biological properties specific for BM micrometastatic cells, however, is technically challenging due to the limited number of target cells usually available for the purpose. This report provides referrals to qualitative gene expression profiling of BM micrometastatic cells enriched by immunomagnetic selection. First, an experimental strategy was used to study regulatory mechanisms involved when BM micrometastatic cells colonize distant organs. The MA-11 cells, originating from BM micrometastases in a breast cancer patient clinically devoid of overt metastatic disease, were injected into immunodeficient rats. Metastatic MA-11 cells were subsequently immunoselected from the resulting in vivo lesions. The selected cell populations were compared to the injected cells by differential display analysis, and several genes possibly involved in tumor cell invasion and proliferation were confirmed as differentially expressed among the various MA-11 cell populations. A direct approach to qualitative gene expression profiling of BM micrometastatic cells was also explored. Carcinoma cells were immunoselected from BM and axillary lymph nodes obtained from breast cancer patients, and the isolated cell populations were compared by differential display analysis. Two candidate genes, identified as factors involved in cellular growth control, appeared as differentially expressed by the target cells from BM. Our study provides detailed information on how to combine an immunomagnetic selection procedure and differential display analysis to reveal gene expression profiles that may characterize BM micrometastatic cells. © 2002 Wiley-Liss, Inc. Key words: bone marrow; micrometastasis; breast cancer; immunomagnetic cell preparation; differential cloningClinical and experimental evidence suggests that epithelial tumor cells are able to disseminate to secondary organs at an early stage of primary tumor development. The red bone marrow (BM) compartment represents an important indicator organ of hematogenous micrometastatic spread of carcinomas. According to current concepts, however, disseminated tumor cells detected in the BM are not able to grow as distant metastatic lesions unless they possess certain biological characteristics, among which the ability of invasion into and proliferation within the target organ is considered highly significant. [1][2][3] The classical, experimental works on mechanisms of tumor metastasis demonstrated that only a small subset of cells within the parental population is capable of metastasizing 4 and that the cellular composition of secondary tumors differs from that of the primaries. 5 Subsequent reports introduced the concept of dynamic heterogeneity, which argues that although the metastatic phenotype is a genetically controlled trait, it is inherently unstable. 6 Indeed, cellular properties that are crucial for initiation of distant tumor growth may be obscured by the heterog...

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Increased expression of T‐plastin gene in cisplatin‐resistant human cancer cells: identification by mRNA differential display

Cited by 44 publications

References 37 publications

Plastin3 Is a Novel Marker for Circulating Tumor Cells Undergoing the Epithelial–Mesenchymal Transition and Is Associated with Colorectal Cancer Prognosis

Plastin3 Is a Novel Marker for Circulating Tumor Cells Undergoing the Epithelial–Mesenchymal Transition and Is Associated with Colorectal Cancer Prognosis

EB-1, a tyrosine kinase signal transduction gene, is transcriptionally activated in the t(1;19) subset of pre-B ALL, which express oncoprotein E2a-Pbx1

Differential display analysis of breast carcinoma cells enriched by immunomagnetic target cell selection: Gene expression profiles in bone marrow target cells

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