Ribonucleotide Reductase Immunoreactivity in Adenocarcinoma Cells and Malignant or Reactive Mesothelial Cells in Serous Effusions

Okamura, Hiroshi; Kamei, Toshiaki; Sakuma, Nobuo; Hanai, Nobuo; Ishihara, Tokuhiro

doi:10.1159/000326506

Cited by 6 publications

(5 citation statements)

References 22 publications

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“…Ribonucleotide reductase M2 (RRM2), a rate-limiting enzyme for DNA synthesis and repair (16,17), was found to be highly expressed in various diseases including gestational trophoblastic disease, breast, pancreatic and gallbladder cancer, which is related to the growth, invasion and chemoresistance of malignant tumors (11,(18)(19)(20). In the present study, RRM2 was detected in 67 pairs of neuroblastoma tissues and adjacent non-cancerous tissues.…”

Section: Discussionmentioning

confidence: 55%

Suppression of RRM2 inhibits cell proliferation, causes cell cycle arrest and promotes the apoptosis of human neuroblastoma cells and in human neuroblastoma RRM2 is suppressed following chemotherapy

Pang

Liu

et al. 2018

Oncol Rep

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Ribonucleotide reductase regulatory subunit M2 (RRM2) is a rate‑limiting enzyme for DNA synthesis and repair. RRM2 has vital roles in controlling the progression of cancer. In the present study, we investigated the RRM2 level in neuroblastoma tissues, analyzed its relationship with clinicopathological characteristics of neuroblastoma patients, and explored the effect of RRM2 on the biological functions of neuroblastoma cells. RRM2 levels in 67 pairs of neuroblastoma and matched adjacent non‑cancerous tissues were detected by qRT‑PCR, and its association with patient clinicopathological features was assessed. Using RRM2 siRNA, the role of RRM2 in cell viability was detected by CCK‑8 assay, and the effects on cell cycle distribution and cell apoptosis were detected by flow cytometry. Hoechst 33342 staining was also performed. For RRM2 protein detection in cells and tissues, western blot analyses were employed. Our results revealed that RRM2 expression was significant higher in neuroblastoma tissues than that noted in adjacent non‑cancerous tissues at both the mRNA and protein levels. The increased RRM2 level was significantly associated with clinical stage. RRM2 levels were suppressed in stage III and IV tumors in the chemotherapy subgroup, compared with levels noted in tumors in the preoperative non‑chemotherapy subgroup. RRM2 siRNA significantly inhibited cell viability in the SH‑5Y5Y cells, induced cell arrest in the G0/G1 phase, and enhanced cell apoptosis. Taken together, overexpression of RRM2 is associated with the genesis and progression of neuroblastoma, and may be a potential chemotherapeutic target.

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Section: Discussionmentioning

confidence: 55%

Suppression of RRM2 inhibits cell proliferation, causes cell cycle arrest and promotes the apoptosis of human neuroblastoma cells and in human neuroblastoma RRM2 is suppressed following chemotherapy

Pang

Liu

et al. 2018

Oncol Rep

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“…The high level of RRM‐2 expression exists in breast cancer and pre‐malignant disease (48) . RRM‐2 immunostaining can be useful as an adjunct for differentiating adenocarcinomas or malignant mesotheliomas from reactive mesothelia in serous effusions (49) .…”

Section: Discussionmentioning

confidence: 99%

The changes of gene expression profiles in hydatidiform mole and choriocarcinoma with hyperplasia of trophoblasts

Cui¹,

Shi²,

Zhou³

et al. 2004

Int J Gynecol Cancer

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The purpose of this study is to investigate changes of gene expression profiles in hydatidiform moles (HM) and choriocarcinoma and to explore causes of trophoblastic hyperplasia. Using cDNA microarray, 4,096 genes were analyzed in two pairs of the tissues of HM versus normal villi and in two pairs of normal primary culture trophoblasts versus JAR cell line of choriocarcinoma. The expressions of two genes in normal villi and HM, as well as in JAR and JEG-3, were examined with the help of immunohistochemistry, immunoblot, and reverse transcriptase-polymerase chain reaction in order to confirm the findings of cDNA microarray. Twenty-four genes were upregulated and 65 genes were downregulated in all HM. Four hundred thirty-three genes were upregulated and 380 genes were downregulated in JAR. Forty-six genes were upregulated in both HM and choriocarcinoma, whereas 13 genes were downregulated. Genes associated with the inhibition of cell proliferation were significantly downregulated, whereas genes associated with cell proliferation, malignant transformation, metastasis, and drug resistance were upregulated. Thymidine kinase-1 (TK-1) and small subunit ribonucleotide reductase (RRM-2) were overexpressed in HM, JAR, and JEG-3. The expressions of TK-1 and RRM-2 in moles were positively correlated with proliferative index of trophoblasts. Our results suggest that altered expression of genes exist in HM and choriocarcinoma. Trophoblastic hyperplasia may be involved in the overexpression of DNA synthetic enzymes.

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“…The high level of RRM-2 expression exists in breast cancer and pre-malignant disease (48) . RRM-2 immunostaining can be useful as an adjunct for differentiating adenocarcinomas or malignant mesotheliomas from reactive mesothelia in serous effusions (49) . According to the initial screening results of cDNA microarray, combining the GTD biologic characters, we analyze the bioinformation of some genes of DNA Synthetic enzymes and detect their expressions.…”

Section: Examination Of Dna Synthesis Enzyme and Trophoblastic Hyperpmentioning

confidence: 99%

The changes of gene expression profiles in hydatidiform mole and choriocarcinoma with hyperplasia of trophoblasts

Cui

Shi

Zhou

et al. 2004

Int J Gynecol Cancer

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Cui JQ, Shi YF, Zhou HJ, Li JQ. The changes of gene expression profiles in hydatidiform mole and choriocarcinoma with hyperplasia of trophoblasts. Int J Gynecol Cancer 2004;14:984-997.The purpose of this study is to investigate changes of gene expression profiles in hydatidiform moles (HM) and choriocarcinoma and to explore causes of trophoblastic hyperplasia. Using cDNA microarray, 4096 genes were analyzed in two pairs of the tissues of HM versus normal villi and in two pairs of normal primary culture trophoblasts versus JAR cell line of choriocarcinoma. The expressions of two genes in normal villi and HM, as well as in JAR and JEG-3, were examined with the help of immunohistochemistry, immunoblot, and reverse transcriptase-polymerase chain reaction in order to confirm the findings of cDNA microarray. Twentyfour genes were upregulated and 65 genes were downregulated in all HM. Four hundred thirty-three genes were upregulated and 380 genes were downregulated in JAR. Forty-six genes were upregulated in both HM and choriocarcinoma, whereas 13 genes were downregulated. Genes associated with the inhibition of cell proliferation were significantly downregulated, whereas genes associated with cell proliferation, malignant transformation, metastasis, and drug resistance were upregulated. Thymidine kinase-1 (TK-1) and small subunit ribonucleotide reductase (RRM-2) were overexpressed in HM, JAR, and JEG-3. The expressions of TK-1 and RRM-2 in moles were positively correlated with proliferative index of trophoblasts. Our results suggest that altered expression of genes exist in HM and choriocarcinoma. Trophoblastic hyperplasia may be involved in the overexpression of DNA synthetic enzymes.

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Ribonucleotide Reductase Immunoreactivity in Adenocarcinoma Cells and Malignant or Reactive Mesothelial Cells in Serous Effusions

Cited by 6 publications

References 22 publications

Suppression of RRM2 inhibits cell proliferation, causes cell cycle arrest and promotes the apoptosis of human neuroblastoma cells and in human neuroblastoma RRM2 is suppressed following chemotherapy

Suppression of RRM2 inhibits cell proliferation, causes cell cycle arrest and promotes the apoptosis of human neuroblastoma cells and in human neuroblastoma RRM2 is suppressed following chemotherapy

The changes of gene expression profiles in hydatidiform mole and choriocarcinoma with hyperplasia of trophoblasts

The changes of gene expression profiles in hydatidiform mole and choriocarcinoma with hyperplasia of trophoblasts

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