Cisplatin-induced apoptosis in non-small-cell lung cancer cells is dependent on Bax- and Bak-induction pathway and synergistically activated by BH3-mimetic ABT-263 in p53 wild-type and mutant cells

Matsumoto, Masaru; Nakajima, Wataru; Seike, Masahiro; Gemma, Akihiko; Tanaka, Nobuyuki

doi:10.1016/j.bbrc.2016.03.053

Cited by 58 publications

(42 citation statements)

References 37 publications

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“…Moreover, PTEN is a well-studied gene that inhibits tumor growth and invasion in nearly all types of human cancers, including gastric cancer, breast cancer, and lung cancer [38–41]. BAK was demonstrated to promote tumor apoptosis and chemosensitivity to chemotherapeutic drugs in non-small-cell lung cancer and gastric cancer [42, 43]. CHD1 was also reported to be a tumor suppressor gene in many human cancers [44, 45].…”

Section: Discussionmentioning

confidence: 99%

Role of ARPC2 in Human Gastric Cancer

Zhang

Liu

et al. 2017

Mediators of Inflammation

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Gastric cancer continues to be the second most frequent cause of cancer deaths worldwide. However, the exact molecular mechanisms are still unclear. Further research to find potential targets for therapy is critical and urgent. In this study, we found that ARPC2 promoted cell proliferation and invasion in the human cancer cell line MKN-28 using a cell total number assay, MTT (3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide) assay, cell colony formation assay, migration assay, invasion assay, and wound healing assay. For downstream pathways, CTNND1, EZH2, BCL2L2, CDH2, VIM, and EGFR were upregulated by ARPC2, whereas PTEN, BAK, and CDH1 were downregulated by ARPC2. In a clinical study, we examined the expression of ARPC2 in 110 cases of normal human gastric tissues and 110 cases of human gastric cancer tissues. ARPC2 showed higher expression in gastric cancer tissues than in normal gastric tissues. In the association analysis of 110 gastric cancer tissues, ARPC2 showed significant associations with large tumor size, lymph node invasion, and high tumor stage. In addition, ARPC2-positive patients exhibited lower RFS and OS rates compared with ARPC2-negative patients. We thus identify that ARPC2 plays an aneretic role in human gastric cancer and provided a new target for gastric cancer therapy.

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Section: Discussionmentioning

confidence: 99%

Role of ARPC2 in Human Gastric Cancer

Zhang

Liu

et al. 2017

Mediators of Inflammation

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“…However, cancer cells survive by adapting to the effects of increasing levels of MCL1 and other anti-apoptotic BCL-2 family proteins. Although some lung cancer cells do not depend on MCL1 for survival 38 , the expression of MCL1 is elevated in most lung cancer cells by various mechanisms (Figure 2). Many reports have shown that suppression of MCL1 increases the sensitivity of lung cancer cells to anticancer drugs 10,18,27 .…”

Section: The Role Of Mcl1 and Its Targeted Therapy In Lung Cancermentioning

confidence: 99%

The anti-apoptotic protein MCL1, a novel target of lung cancer therapy

Tanaka¹

2017

J Cancer Treat & Diagnosis

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Evasion of apoptosis is one of the typical hallmarks of cancer and a major mechanism for cancer development, tumor growth, and acquisition of resistance to chemotherapy. The anti-apoptotic Bcl-2 protein family, particularly MCL1 and BCL-XL, play an important role in acquisition of apoptosis evasion. MCL1 is a highly unstable protein that is constantly degraded by the ubiquitinproteasome system. An increase in MCL1 protein has been reported in many cancers, including lung cancer, through high mRNA expression or impairment of its degradation systems. To date, much evidence has shown that MCL1 is important for cancer cell survival and drug resistance in lung cancers. In this review, we discuss the role and mechanism of high MCL1 expression in lung cancer.

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“…Compared with Bcl-2, Bcl-xL can inhibit DISC formation and presentation and excitation of Bid, which indicates that Bcl-xL can inhibit upstream signaling in TNF-induced apoptosis more effectively than Bcl-2 (20). Overexpression of Bcl-xL can inhibit disruption of the DeltaPsim (inner mitochondrial membrane potential) and reduce generation of ROS and MMP (21). The growth-promoting activity of Bcl-xL has been explored in a series of overexpression and gene knockout studies (6,22).…”

Section: Discussionmentioning

confidence: 99%

The effect of miR-146a on STAT1 expression and apoptosis in acute lymphoblastic leukemia Jurkat cells

Wang¹,

Guo²,

Suo³

et al. 2016

Oncology Letters

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The effect of miR-146a-dependent regulation of STAT1 on apoptosis in acute lymphoblastic leukemia (ALL) Jurkat cells was investigated. The miR-146a mimic and miR-146a inhibitor vectors were constructed in vitro, and experimental grouping was as follows: Control group (untreated Jurkat cells), empty vector group (Jurkat cells transfected with empty vector), agonist group (Jurkat cells transfected with miR-146a mimic) and the inhibitor group (Jurkat cells transfected with miR-146a inhibitor). Western blot analysis was used to observe the expression, respectively, of STAT1, p-STAT1 and Bcl-xL, and flow cytometry was used to test apoptosis in Jurkat cells. STAT1 and p-STAT1 expression in the agonist group was higher than that in the control and empty vector groups, but lower in the inhibitor group, and differences were statistically significant (P<0.05). The rate of apoptosis in the agonist group was significantly higher than that of the control group and blank vector group, and it was significantly lower in the inhibitor group (P<0.05). As a tumor suppressor, miR-146a can regulate expression of apoptosis-promoting factor STAT1, and anti-apoptosis factor Bcl-xL, and is able to promote apoptosis of ALL Jurkat cells.

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Cisplatin-induced apoptosis in non-small-cell lung cancer cells is dependent on Bax- and Bak-induction pathway and synergistically activated by BH3-mimetic ABT-263 in p53 wild-type and mutant cells

Cited by 58 publications

References 37 publications

Role of ARPC2 in Human Gastric Cancer

Role of ARPC2 in Human Gastric Cancer

The anti-apoptotic protein MCL1, a novel target of lung cancer therapy

The effect of miR-146a on STAT1 expression and apoptosis in acute lymphoblastic leukemia Jurkat cells

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