scholarly journals 20(S)-Ginsenoside Rg3 Promotes HeLa Cell Apoptosis by Regulating Autophagy

Molecules ◽  
2019 ◽  
Vol 24 (20) ◽  
pp. 3655 ◽  
Author(s):  
Bian ◽  
Zhao ◽  
Li ◽  
Lu ◽  
Wang ◽  
...  
Keyword(s):  
Hela Cell ◽  
Cell Apoptosis ◽  
Cell Counting ◽  
Ginsenoside Rg3 ◽  
Species Determination ◽  
Protein Levels ◽  
Autophagy Inhibitor ◽  
Autophagy Induction ◽  
Apoptotic Pathways ◽  
Induced Apoptosis

20(S)-Ginsenoside Rg3 (GRg3) has various bioactivities including anti-cancer effects and inhibition of autophagy. However, no reports have investigated the appearance of autophagy or the connection between autophagy and apoptosis in HeLa cells treated with 20(S)-GRg3. Cell viability was measured by CCK-8 (cell counting kit-8) assays. Apoptosis and the cell cycle were analyzed by Hoechst 33342 staining and flow cytometry. Apoptotic pathways were examined by ROS (reactive oxygen species) determination and rhodamine 123 assays. Western blot analysis was used to determine changes in protein levels. Autophagy induction was monitored by acidic vesicular organelle staining and EGFP-LC3 transfection. 20(S)-GRg3 inhibited autophagy of cells in a starved state, making it impossible for cells to maintain a steady state through autophagy, and then induced apoptosis. 20(S)-GRg3 blocked the late stage of autophagy (fusion of lysosomes and degradation of autophagic lysosomes), including a decrease in acidic vesicular organelle fluorescence, increased LC3 I–II conversion, accumulation of EGFP-LC3 fluorescence, GFP-mRFP-LC3 red-green fluorescence ratio, degradation of the substrate p62, and loss of the balance between autophagy and apoptosis, which induced apoptosis. ROS increased, the mitochondrial membrane potential decreased, apoptotic inducer AIF was released from mitochondria, and nuclear transfer occurred, triggering a series of subsequent apoptotic events. Autophagy inducer rapamycin inhibited the apoptosis induced by 20(S)-GRg3, whereas autophagy inhibitor BA1 promoted apoptosis induced by 20(S)-GRg3. Therefore, 20(S)-GRg3 promoted HeLa cell apoptosis by regulating autophagy. In the autophagic state, 20(S)-GRg3 can be used as a novel autophagy inhibitor in synergy with tumor-blocking therapies such as chemotherapy, which supports its application in the medical field.

scholarly journals Skullcapflavone I protects cardiomyocytes from hypoxia-caused injury through up-regulation of lincRNA-ROR

2019 ◽  
Vol 33 ◽  
pp. 205873841985753 ◽  
Author(s):  
Zhenxiao Zhang ◽  
Hui Li ◽  
Mingyang Liu ◽  
Jianshuai He ◽  
Xiaotian Zhang ◽  
...  
Keyword(s):  
Cell Apoptosis ◽  
Cell Injury ◽  
Mitogen Activated Protein Kinase ◽  
Cell Counting ◽  
H9c2 Cell ◽  
Erk Pathway ◽  
H9c2 Cells ◽  
Scutellaria Baicalensis Georgi ◽  
Protein Levels

Myocardial infarction (MI) is a serious heart disease in which cardiomyocytes are damaged, caused by hypoxia. This study explored the possible protective activity of Skullcapflavone I (SF I), a flavonoid isolated from the root of Scutellaria baicalensis Georgi, on hypoxia-stimulated cardiomyocytes cell injury in vitro. Viability and apoptosis of H9c2 cells and primary cardiomyocytes were tested using cell counting kit–8 (CCK-8) assay and Guava Nexin Reagent, respectively. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to measure the long non-coding RNA regulator of reprogramming (lincRNA-ROR) expression. si-ROR was transfected to knockdown lincRNA-ROR. Western blotting was conducted to assess the protein levels of key molecules related to cell proliferation, apoptosis, and mitogen-activated protein kinase/extracellular signal–regulated kinase (MEK/ERK) pathway. We discovered that hypoxia stimulation obviously reduced H9c2 cell and primary cardiomyocytes’ viability and proliferation, but promoted cell apoptosis. SF I treatment mitigated the cell viability and proliferation inhibition, as well as cell apoptosis caused by hypoxia. Moreover, SF I promoted the hypoxia-caused up-regulation of lincRNA-ROR in H9c2 cells and primary cardiomyocytes. Knockdown of lincRNA-ROR reversed the influence of SF I on hypoxia-stimulated H9c2 cells and primary cardiomyocytes. Besides, SF I activated MEK/ERK pathway in H9c2 cells and primary cardiomyocytes via up-regulating lincRNA-ROR. To sum up, our research verified the beneficial activity of SF I on hypoxia-caused cardiomyocytes injury. SF I protected cardiomyocytes from hypoxia-caused injury through up-regulation of lincRNA-ROR and activation of MEK/ERK pathway.

scholarly journals Apoptosis Triggered by Myc-Induced Suppression of Bcl-XL or Bcl-2 Is Bypassed during Lymphomagenesis

2001 ◽  
Vol 21 (15) ◽  
pp. 5063-5070 ◽  
Author(s):  
Christine M. Eischen ◽  
David Woo ◽  
Martine F. Roussel ◽  
John L. Cleveland
Keyword(s):  
Protein Synthesis ◽  
Transgenic Mice ◽  
Tumor Cells ◽  
De Novo ◽  
Apoptotic Pathway ◽  
Antiapoptotic Protein ◽  
Protein Levels ◽  
Apoptotic Pathways ◽  
Induced Apoptosis ◽  
De Novo Protein Synthesis

ABSTRACT Enforced Bcl-2 expression inhibits Myc-induced apoptosis and cooperates with Myc in transformation. Here we report that the synergy between Bcl-2 and Myc in transforming hematopoietic cells in fact reflects a Myc-induced pathway that selectively suppresses the expression of the Bcl-XL or Bcl-2 antiapoptotic protein. Myc activation suppresses Bcl-XL RNA and protein levels in cultures of primary myeloid and lymphoid progenitors, and Bcl-XL and Bcl-2 expression is inhibited by Myc in precancerous B cells from Eμ-myc transgenic mice. The suppression of bcl-X RNA levels by Myc requires de novo protein synthesis, indicating that repression is indirect. Importantly, the suppression of Bcl-2 or Bcl-XL by Myc is corrupted during Myc-induced tumorigenesis, as Bcl-2 and/or Bcl-XLlevels are markedly elevated in over one-half of all lymphomas arising in Eμ-myc transgenic mice. Bcl-2 and/or Bcl-XL overexpression did not correlate with loss of ARF or p53 function in tumor cells, indicating that these two apoptotic pathways are inactivated independently. Therefore, the suppression of Bcl-XL or Bcl-2 expression represents a physiological Myc-induced apoptotic pathway that is frequently bypassed during lymphomagenesis.

scholarly journals Nobiletin, a hexamethoxyflavonoid from citrus pomace, attenuates G1 cell cycle arrest and apoptosis in hypoxia-induced human trophoblast cells of JEG-3 and BeWo via regulating the p53 signaling pathway

2021 ◽  
Author(s):  
Mengling Zhang ◽  
Jian Liu ◽  
Rui Zhang ◽  
Zengenni Liang ◽  
Shenghua Ding ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Western Blot ◽  
Blot Analysis ◽  
Cell Apoptosis ◽  
Western Blot Analysis ◽  
P53 Protein ◽  
Human Trophoblast ◽  
Protein Levels ◽  
Bewo Cells ◽  
Induced Apoptosis

Background: Hypoxia is associated with abnormal cell apoptosis in trophoblast cells, which causes fetal growth restriction and related placental pathologies. Few effective methods for the prevention and treatment of placenta-related diseases exist. Natural products and functional foods have always been a rich source of potential anti-apoptotic drugs. Nobiletin (NOB), a hexamethoxyflavonoid derived from the citrus pomace, shows an anti-apoptotic activity, which is a non-toxic constituent of dietary phytochemicals approved by the Food and Drug Administration. However, their effects on hypoxia-induced human trophoblast cells have not been fully studied. Objective: The aim of this study was to investigate the protective effects of NOB on hypoxia-induced apoptosis of human trophoblast JEG-3 and BeWo cells, and their underlying mechanisms. Design: First, the protective effect of NOB on hypoxia-induced apoptosis of JEG-3 and BeWo cells was studied. Cell viability and membrane integrity were determined by CCK-8 assay and lactate dehydrogenase activity, respectively. Real Time Quantitative PCR (RT-qPCR) and Western blot analysis were used to detect the mRNA and protein levels of HIF1α. Propidium iodide (PI)-labeled flow cytometry was used to detect cell cycle distribution. Cell apoptosis was detected by flow cytometry with Annexin V-FITC and PI double staining, and the expression of apoptosis marker protein cl-PARP was detected by Western blot analysis. Then, the molecular mechanism of NOB against apoptosis was investigated. Computer molecular docking and dynamics were used to simulate the interaction between NOB and p53 protein, and this interaction was verified in vitro by Ultraviolet and visible spectrum (UV-visible spectroscopy), fluorescence spectroscopy and circular dichroism. Furthermore, the changes in the expression of p53 signaling pathway genes and proteins were detected by RT-qPCR and Western blot analysis, respectively. Results: Hypoxia treatment resulted in a decreased cell viability and cell membrane integrity in JEG-3 and BeWo cell lines, and an increased expression of HIF1α, cell cycle arrest in the G1 phase, and massive cell apoptosis, which were alleviated after NOB treatment. Molecular docking and dynamics simulations found that NOB spontaneously bonded to human p53 protein, leading to the change of protein conformation. The intermolecular interaction between NOB and human p53 protein was further confirmed by UV-visible spectroscopy, fluorescence spectroscopy and circular dichroism. After the treatment of 100 μM NOB, a down-regulation of mRNA and protein levels of p53 and p21 and an up-regulation of BCL2/BAX mRNA and protein ratio were observed in JEG-3 cells; however, there was also a down-regulation of mRNA and protein levels observed for p53 and p21 in BeWo cells after the treatment of NOB. The BCL2/BAX ratio of BeWo cells did not change after the treatment of 100 μM NOB. Conclusion: NOB attenuated hypoxia-induced apoptosis in JEG-3 and BeWo cell lines and might be a potential functional ingredient to prevent pregnancy-related diseases caused by hypoxia-induced apoptosis. These findings would also suggest the exploration and utilization of citrus resources, and the development of citrus industry.

scholarly journals LncRNA KCNQ1OT1 promotes the development of diabetic nephropathy by regulating miR-93-5p/ROCK2 axis

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Li Zhao ◽  
Huaqian Chen ◽  
Lin Wu ◽  
Zhengdong Li ◽  
Ren Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Diabetic Nephropathy ◽  
Mesangial Cells ◽  
Coiled Coil ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Glomerular Mesangial Cells ◽  
Cell Models ◽  
Protein Levels ◽  
Induced Apoptosis

Abstract Background Long non-coding RNAs (lncRNAs) have been reported to play vital roles in diabetic nephropathy (DN). The aim of this study was to explore the function of mechanism of lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) in DN. Methods DN cell models were established using high glucose (HG) treatment in human glomerular mesangial cells (HGMC) and human renal glomerular endothelial cells (HRGEC). The expression levels of KCNQ1OT1, microRNA-93-5p (miR-93-5p), and Rho associated coiled-coil containing protein kinase 2 (ROCK2) mRNA was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell Counting Kit-8 (CCK-8) assay and flow cytometry were used to detect cell proliferation and apoptosis, respectively. ROCK2 and apoptosis/fibrosis-related protein levels were examined by western blot. The predicted interaction between miR-93-5p and KCNQ1OT1 or ROCK2 was verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Results KCNQ1OT1 was upregulated in DN patients and DN cell models. KCNQ1OT1 knockdown inhibited cell proliferation and fibrosis and induced apoptosis in DN cell models. MiR-93-5p was a direct target of KCNQ1OT1, and miR-93-5p inhibition restored the KCNQ1OT1 knockdown-mediated effects on cell proliferation, fibrosis and apoptosis in DN cell models. In addition, ROCK2 was identified as a target of miR-93-5p, and miR-93-5p overexpression suppressed cell proliferation and fibrosis and accelerated apoptosis by targeting ROCK2 in DN cell models. Moreover, KCNQ1OT1 regulated ROCK2 expression by binding to miR-93-5p. Conclusion KCNQ1OT1 knockdown inhibited cell proliferation and fibrosis and induced apoptosis in DN by regulating miR-93-5p/ROCK2 axis, providing potential value for the treatment of DN.

scholarly journals Cullin3 Aggravates The Inflammatory Response of PDLSCs Via Regulation of Shh Signaling and Nrf2

2021 ◽  
Author(s):  
Wanhong Chen ◽  
Jiangling Su ◽  
Shixiong Cai ◽  
Chun Shi
Keyword(s):  
Cell Viability ◽  
Cell Apoptosis ◽  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tunel Staining ◽  
Western Blots ◽  
Alizarin Red ◽  
Shh Signaling ◽  
Protein Levels ◽  
Alkaline Phosphatase Staining

Abstract Objective: Sonic Hedgehog (Shh) was found to be correlated with inflammation degree of patients with periodontitis. Cullin3 is an important ubiquitin ligase for controlling Shh signaling. In this study, we exerted ourselves to clarify the roles of Shh and Cullin3 in P. gingivalis-LPS (Pg-LPS)-treated periodontal ligament stem cells (PDLSCs). Methods: Cell viability was detected using cell counting kit-8 (CCK-8). The inflammatory cytokines of PDLSCs were estimated by enzyme-linked immunosorbent assay (ELISA). The protein levels of Shh, Gli1 and NF-E2-related factor2 (Nrf2) were determined via western blots. Alkaline phosphatase staining and Alizarin red staining were performed to evaluate the differentiation and mineralization capabilities of PDLSCs. The apoptotic cells were screened by TUNEL staining. Results: Pg-LPS inhibited cell viability and triggered inflammation of PDLSCs. Overexpression of Cullin3 impeded the differentiation and mineralization capabilities of PDLSCs. Moreover, Cullin3 overexpression aggravated inflammation and cell apoptosis induced by Pg-LPS. Of note, while the protein levels of Shh, Gli1 and Nrf2 were elevated in PDLSCs treated with Pg-LPS, overexpression of Cullin3 decreased the expressions of them. Conclusion: Shh/Gli1 and Nrf2 were involved in the inflammation and cell apoptosis of PDLSCs, which was dominated by Cullin3.

NO66 overexpression rescues ethanol-induced cell apoptosis in human AC16 cardiomyocytes by suppressing PTEN and activating the PI3K/Akt signaling

2020 ◽  
Vol 52 (10) ◽  
pp. 1093-1101
Author(s):  
Hanyu Deng ◽  
Bo Yu ◽  
Yang Yu ◽  
Ge Tian ◽  
Liu Yang
Keyword(s):  
Cell Apoptosis ◽  
Cell Injury ◽  
Membrane Damage ◽  
Annexin V ◽  
B Cell Lymphoma ◽  
Alcohol Exposure ◽  
Ethanol Exposure ◽  
Cell Counting ◽  
Pi3k Inhibitor Ly294002 ◽  
Induced Apoptosis

Abstract Previously, Nucleolar protein 66 (NO66) was reported to be closely associated with alcohol exposure-induced injury. However, the role of NO66 in alcohol-induced cytotoxicity remains unclear. In this study, we explored the potential effect and mechanism of NO66 on ethanol-induced apoptosis in human AC16 cardiomyocytes. The AC16 cell lines with NO66 and phosphatase and tensin homolog (PTEN) overexpression were constructed. Cell counting kit-8 (CCK-8), lactate dehydrogenase (LDH) assay, Annexin V-FITC/PI staining, and flow cytometry were used to evaluate the cell viability, membrane damage, and apoptosis, respectively. Quantitative real-time PCR (qRT-PCR) and western blot analysis were applied to measure mRNA and protein expression. The results showed that acute ethanol exposure markedly augmented cytotoxicity and reduced NO66 level in AC16 cardiomyocytes. Overexpression of NO66 partially reversed ethanol-induced apoptosis. NO66 upregulation reversed the decrease in phosphorylation of protein kinase B (Akt) and B-cell lymphoma-2/Bcl-2-associated x (Bcl-2/Bax) ratio and the increase in PTEN, p53, and caspase-3 activity induced by ethanol treatment. Meanwhile, the application of PI3K inhibitor (LY294002) and PTEN overexpression attenuated the inhibition efficiency of NO66 on cell apoptosis. In addition, PTEN overexpression weakened the effect of NO66 on PI3K/Akt activation, without affecting the level of NO66. Our data suggested that NO66 overexpression might play an anti-apoptotic role in ethanol-induced cell injury via reducing PTEN and upregulating the PI3K/Akt pathway.

scholarly journals YCl3 Promotes Neuronal Cell Death by Inducing Apoptotic Pathways in Rats

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Yechun Ding ◽  
Yuantong Tian ◽  
Zhaoyi Zeng ◽  
Ping Shuai ◽  
Haiying Lan ◽  
...  
Keyword(s):  
Cell Death ◽  
Rare Earth ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Free Access ◽  
Protein Levels ◽  
Access To Water ◽  
Apoptotic Pathways

The pollutants rare earth elements (REEs) have posed great threats to human health. To investigate the cytotoxicity of yttrium (Y), a model that rats have free access to water containing YCl3 for 6 months is utilized. The results showed that YCl3 treatment promoted neuronal cell apoptosis by upregulating the proapoptotic factors Bax, caspase-3, Cyto c, and DAPK and by downregulating the antiapoptotic factors Bcl-2 and XIAP at both mRNA and protein levels. Conclusively, YCl3 exhibited cytotoxicity and promoted neuronal cell death by the induction of apoptotic pathways.

scholarly journals Linc-KIAA1737–2 promoted LPS-induced HK-2 cell apoptosis by regulating miR-27a-3p/TLR4/NF-κB axis

2021 ◽  
Author(s):  
Ming Hu ◽  
Jing Wei ◽  
Liu Yang ◽  
Jianhua Xu ◽  
Zhaofeng He ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Epithelial Cells ◽  
Cell Apoptosis ◽  
Kidney Injury ◽  
Luciferase Assay ◽  
Tubular Epithelial Cells ◽  
Protein Levels ◽  
Proximal Tubular Epithelial Cells ◽  
Proximal Tubular ◽  
Induced Apoptosis

AbstractInflammation and renal cell apoptosis participate in sepsis-induced acute kidney injury. Previous research found the upregulation of long non-coding RNA Linc-KIAA1737–2 in hypoxia- or inflammation-challenged human proximal tubular epithelial cells, but its role in sepsis-induced acute kidney injury is underexplored. In this research, we found that Linc-KIAA1737–2 could be upregulated in HK-2 human proximal tubular epithelial cells by LPS treatment, and knock-down of this lncRNA significantly attenuated LPS-induced apoptosis in HK-2 cells, while its overexpression showed opposite effect. MiR-27a-3p was confirmed to interact with Linc-KIAA1737–2 in HK-2 cells by RNA pull-down and dual-luciferase assay. MiR-27a-3p mimic transfection significantly attenuated LPS-induced HK-2 cell apoptosis by downregulating the protein levels of TLR4 and NF-κB, which was overturned by overexpression of Linc-KIAA1737–2. Our results suggested that Linc-KIAA1737–2 could promote LPS-induced apoptosis in HK-2 cells, and presumably sepsis-induced acute kidney injury, by regulating the miR-27a-3p/TLR4/NF-κB axis.

scholarly journals Degradation of Mcl-1 through GSK-3β Activation Regulates Apoptosis Induced by Bufalin in Non-Small Cell Lung Cancer H1975 Cells

2017 ◽  
Vol 41 (5) ◽  
pp. 2067-2076 ◽  
Author(s):  
Xiao-hong Kang ◽  
Jing-hang Zhang ◽  
Qing-qin Zhang ◽  
Yan-hui Cui ◽  
Ying Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Cell Apoptosis ◽  
Small Cell ◽  
Cell Counting ◽  
Dependent Manner ◽  
Small Cell Lung ◽  
Gsk 3Β ◽  
Induced Apoptosis

Background/Aims: Mcl-1, an anti-apoptotic Bcl-2 family member, is often overexpressed in non-small cell lung cancer (NSCLC). Bufalin has been reported to induce apoptosis in various tumor cells. However, there is no report showing that bufalin could downregulate Mcl-1 expression in NSCLC. Methods: Cell proliferation was analyzed by cell counting kit-8 (CCK-8) assay in H1975 cells. Cell apoptosis was detected by flow cytometry. Mcl-1 mRNA was detected by RT-PCR. The expression of apoptosis-associated proteins in H1975 cells was detected by western blotting. The levels of Mcl-1 ubiquitination and NOXA were analyzed by Immunoprecipitation assay. Results: Cell growth was inhibited by bufalin in a time and dose-dependent manner. Bufalin induced apoptosis in NSCLC cells by activating caspase cascades and downregulating Mcl-1 expression. However, overexpression of Mcl-1 diminished bufalin-induced apoptosis. Furthermore, bufalin did not reduce Mcl-1 mRNA expression in H1975 cells, but strongly promoted Mcl-1 protein degradation. Proteasome inhibitor MG132 markedly prevented the degradation of Mcl-1 and blocked bufalin-induced Mcl-1 reduction. Bufalin did not significantly affect NOXA protein levels, but downregulated the expression of p-GSK-3β. GSK-3 inhibitor and GSK-3β siRNA resulted in increased levels of Mcl-1 and reversed the bufalin-induced Mcl-1 degradation. Conclusion: Bufalin induced cell apoptosis in H1975 cells may be through downregulation of Mcl-1. Proteasomal degradation of Mcl-1 via GSK-3β activation was involved in bufalin-induced apoptosis.

OSI-027 alleviates oxaliplatin chemoresistance in gastric cancer cells by suppressing P-gp induction

2020 ◽  
Vol 20 ◽  
Author(s):  
En Xu ◽  
Hao Zhu ◽  
Feng Wang ◽  
Ji Miao ◽  
Shangce Du ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Mammalian Target Of Rapamycin ◽  
Cell Counting ◽  
Gastric Cancer Cells ◽  
Ags Cells ◽  
Dual Inhibitor ◽  
Induced Apoptosis

: Gastric cancer is one of the most common malignancies worldwide and the third leading cause of cancer-related death. In the present study, we investigated the potential activity of OSI-027, a potent and selective mammalian target of rapamycin complex 1/2 (mTOR1/2) dual inhibitor, alone or in combination with oxaliplatin against gastric cancer cells in vitro. Cell counting kit-8 assays and EdU staining were performed to examine the proliferation of cancer cells. Cell cycle and apoptosis were detected by flow cytometry. Western blot was used to detect the elements of the mTOR pathway and Pgp in gastric cancer cell lines. OSI-027 inhibited the proliferation of MKN-45 and AGS cells by arresting the cell cycle in the G0/G1 phase. At the molecular level, OSI-027 simultaneously blocked mTORC1 and mTORC2 activation, and resulted in the downregulation of phosphor-Akt, phpspho-p70S6k, phosphor-4EBP1, cyclin D1, and cyclin-dependent kinase4 (CDK4). Additionally, OSI-027 also downregulated P-gp, which enhanced oxaliplatin-induced apoptosis and suppressed multidrug resistance. Moreover, OSI-027 exhibited synergistic cytotoxic effects with oxaliplatin in vitro, while a P-gp siRNA knockdown significantly inhibited the synergistic effect. In summary, our results suggest that dual mTORC1/mTORC2 inhibitors (e.g., OSI-027) should be further investigated as a potential valuable treatment for gastric cancer.

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