Suppression of myeloid cell leukemia-1 (Mcl-1) enhances chemotherapy-associated apoptosis in gastric cancer cells

Akagi, Hideko; Higuchi, Hajime; Sumimoto, Hidetoshi; Igarashi, Toru; Kabashima, Ayano; Mizuguchi, Hiroyuki; Izumiya, Motoko; Sakai, Gen; Adachi, Masayuki; Funakoshi, Shinsuke; Nakamura, Shoko; Hamamoto, Yasuo; Kanai, Takanori; Takaishi, Hiromasa; Kawakami, Yutaka; Hibi, Toshifumi

doi:10.1007/s10120-012-0153-6

Cited by 57 publications

(43 citation statements)

References 33 publications

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“…In contrast, neither NC siRNA nor lipofectamine treatment changed the impact of chemotherapy, which supports the specific effect of siMcl-1. These results are in agreement with previous reports using other tumor cells (Kano et al, 2009, Akagi et al, 2013. The above-mentioned results confirm that the presence of anti-apoptotic Mcl-1 protein is required for the survival and development of chemoresistance in the HL-60 cell line.…”

Section: Discussionsupporting

confidence: 93%

“…Mcl-1 mainly inhibits the intrinsic pathway by the sequestering and neutralization of pro-apoptotic Bcl-2 family members such as Bak, Bax and Bim, thereby preserving mitochondria integrity. This action blocks the release of cytochrome c from the inner mitochondrial membrane space that is required for caspase activation and next apoptotic events (Warr and Shore, 2008;Zhang et al, 2012;Akagi et al, 2013). Recent studies on melanoma cells have indicated that up-regulation of Mcl-1 inhibited the death receptor pathway of apoptosis (Chetoui et al, 2008;Boisvert-Adamo et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

“…As most of the chemotherapy agents exert their anti-tumor effects by triggering apoptosis, new approaches for cancer treatment have focused on targeting mediators of this pathway (High et al, 2010;Akagi et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, some reports have indicated that Mcl-1 is needed for the function of hematopoetic cell systems and survival of tumor cells (Brunelle et al, 2009;Yecies et al, 2010;Glaser et al, 2012). Studies have shown that Mcl-1 is overexpressed in various malignancies and downregulation of this protein by antisense oligonucleotide (ASO) or RNA interference (RNAi) technology induced apoptosis and sensitized tumor cells to anti-cancer agents (Chetoui et al, 2008;Skoda et al, 2008;Warr and Shore, 2008;Quinn et al, 2011;Akagi et al, 2013). Moreover, elevated expression of Mcl-1 at the time of leukemic relapse, offers a possible explanation to the role of this protein in the survival of leukemia cells after chemotherapy (Kaufmann et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

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Down-Regulation of Mcl-1 by Small Interference RNA Induces Apoptosis and Sensitizes HL-60 Leukemia Cells to Etoposide

Karami¹,

Baradaran²,

Esfehani³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Down-Regulation of Mcl-1 by Small Interference RNA Induces Apoptosis and Sensitizes HL-60 Leukemia Cells to Etoposide

Karami¹,

Baradaran²,

Esfehani³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…Although a number of conventional therapeutic methods, including surgical excision and chemotherapy achieve satisfactory therapeutic effects for patients with early GC, a greater number of patients with GC at an advanced stage have poor prognosis (3). Therefore, despite increasing knowledge of the genetic and biochemical basis of GC, it is also essential to search for novel therapeutic targets and to develop more effective diagnostic and treatment methods.…”

Section: Introductionmentioning

confidence: 99%

Anti-cancer effect of low dose of celecoxib may be associated with lnc-SCD-1:13 and lnc-PTMS-1:3 but not COX-2 in NCI-N87 cells

Song

Shu

et al. 2017

Oncology Letters

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Abstract. In order to investigate the mechanism of celecoxib and whether long non-coding RNAs (lncRNAs) were involved in the effects of celecoxib treatment in NCI-N87 cells, NCI-N87 cells were treated with 15, 30 and 60 µM celecoxib and an MTT assay was performed to assess cell viability. Following treatment with 15 µM celecoxib, the cell cycle and apoptosis were analyzed by flow cytometry, and the mRNA levels of lnc-SCD-1:13, lnc-PTMS-1:3, cyclooxygenase-2 (COX-2), integrin α3 (ITGA3) and DSH homolog 1 (DVL1) were detected by reverse transcription quantitative PCR (RT-qPCR) in NCI-N87 cells. MTT analysis demonstrated that celecoxib significantly inhibited cell viability in treated cells compared with untreated cells. Flow cytometry analysis revealed that, compared with untreated cells, the percentage of cells in the G 0 /G 1 phase was significantly increased, and the percentage of cells in the S and G 2 phase was decreased. In addition, the percentage of early and late apoptotic cells was increased in cells treated with 15 µM celecoxib compared with the control. RT-qPCR analysis also demonstrated that the mRNA levels of lnc-SCD-1:13, lnc-PTMS-1:3, ITGA3 and DVL1 were increased following treatment with celecoxib (15 µM; P<0.05). However, there were no significant differences in the expression of COX-2 mRNA between cells treated with celecoxib (15 µM) and untreated cells. The present study demonstrated that a low dose of celecoxib may be involved in regulating cell growth independent of COX-2 in NCI-N87 cells. Furthermore, ITGA3 and/or DVL1 co-expressed with lnc-SCD-1:13 and lnc-PTMS-1:3 may be associated with the effects of treatment with a low dose of celecoxib in NCI-N87 cells. IntroductionGastric cancer (GC) is a common malignancy worldwide, characterized by high invasiveness and aggressiveness (1).It is estimated that there are ~990,000 new cases of GC and that ~738,000 succumb from this type of cancer per year (2). Although a number of conventional therapeutic methods, including surgical excision and chemotherapy achieve satisfactory therapeutic effects for patients with early GC, a greater number of patients with GC at an advanced stage have poor prognosis (3). Therefore, despite increasing knowledge of the genetic and biochemical basis of GC, it is also essential to search for novel therapeutic targets and to develop more effective diagnostic and treatment methods.A series of studies have reported that nonsteroidal anti-inflammatory drugs (NSAIDs) have an anti-cancer effect in various types of cancer, including breast cancer (4), esophageal cancer (5), colorectal cancer (6), prostate cancer (7) and GC (8). In addition to aspirin, celecoxib, a cyclooxygenase-2 (COX-2) inhibitor, has been demonstrated to be involved in uncontrolled cell proliferation, apoptosis, angiogenesis and metastasis (9,10). Previous studies have suggested that celecoxib is able to induce cell apoptosis through the phosphoinositide 3 kinase/Akt signaling pathway (11) and to inhibit invasion through the adenine nucleotide translocator-...

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ZIPK activates the IL‐6/STAT3 signaling pathway and promotes cisplatin resistance in gastric cancer cells

Fan

Qiao

et al. 2021

FEBS Open Bio

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Gastric cancer is one of the most common malignant cancers globally. Chemotherapy resistance remains a major obstacle in the treatment of gastric cancer, and the molecular mechanisms underlying drug resistance are still not well understood. We previously reported that Zipper interacting protein kinase (ZIPK), also known as death‐associated protein kinase3, exerts an oncogenic effect on gastric cancer via activation of Akt/NF‐κB signaling and promotion of stemness. Here, we explored the roles of ZIPK in cisplatin resistance. We report that ZIPK enhances cell proliferation and invasion and reduces the antitumor activity of cisplatin in gastric cancer. In addition, our western blot data suggest that ZIPK activated the IL‐6/STAT3 signaling pathway. Furthermore, ZIPK increased the expression of IL‐6 and multidrug‐resistance genes. Using the STAT3 inhibitor stattic to block the IL‐6/STAT3 signaling pathway strongly increased the sensitivity of ZIPK‐expressed cells to cisplatin. In conclusion, ZIPK may play a role in cisplatin resistance through activation of the IL‐6/ STAT3 signaling pathway. Inhibition of STAT3 in gastric cancer overexpressing ZIPK might have potential to improve the efficacy of cisplatin.

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Suppression of myeloid cell leukemia-1 (Mcl-1) enhances chemotherapy-associated apoptosis in gastric cancer cells

Cited by 57 publications

References 33 publications

Down-Regulation of Mcl-1 by Small Interference RNA Induces Apoptosis and Sensitizes HL-60 Leukemia Cells to Etoposide

Down-Regulation of Mcl-1 by Small Interference RNA Induces Apoptosis and Sensitizes HL-60 Leukemia Cells to Etoposide

Anti-cancer effect of low dose of celecoxib may be associated with lnc-SCD-1:13 and lnc-PTMS-1:3 but not COX-2 in NCI-N87 cells

ZIPK activates the IL‐6/STAT3 signaling pathway and promotes cisplatin resistance in gastric cancer cells

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