scholarly journals SSRP1 Affects Growth and Apoptosis of Gastric Cancer Cells Through AKT Pathway

2021 ◽  
Author(s):  
Tongyu Tang ◽  
Guohua Jin ◽  
Ruihong Zhao ◽  
Jianguang Zhang ◽  
Tingting Cao
Keyword(s):  
Gastric Cancer ◽  
Survival Rate ◽  
Signaling Pathway ◽  
Colony Formation ◽  
Akt Signaling ◽  
Proliferative Capacity ◽  
Akt Signaling Pathway ◽  
Ags Cells ◽  
Qrt Pcr ◽  
And Migration

Background: We aimed to figure out the SSRP1's potential influence on the apoptosis and proliferation of gastric cancer (GC) cells and its regulatory mechanism. Methods: SSRP1 expression in GC cells and tissues was detected via quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The interrelation between clinicopathological characteristics of GC patients and SSRP1 expression was analyzed via χ2 test, and the correlation between SSRP1 expression and overall survival rate was analyzed using Kaplan-Meier survival analysis. After knockdown of SSRP1 in AGS cells, the SSRP1 expression, colony formation ability, cell viability, cell cycle changes, apoptosis rate, and migration and invasion ability were detected through qRT-PCR, colony formation assay, CCK8 assay, flow cytometry and transwell test, respectively. Finally, the effects of down-regulation of SSRP1 on the expressions of phosphorylated-protein kinase B (p-AKT), B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax) were explored using Western blotting. Results: SSRP1 displayed a high expression in GC cells and tissues. SSRP1 expression was closely interrelated to the TNM stage, lymph node metastasis and tumor size. The survival rate of patients was markedly shorter in high expression group than the lower expression group. After the knockdown of SSRP1 in cells, the viability and colony formation ability of AGS cells were inhibited. In addition, cell ration in the G1 phase was increased, while that in the S phase declined, and the cell invasion and migration were obviously weakened. It was found from Western blotting that the knockdown of SSRP1 could evidently suppress the protein levels of Bcl-2 and p-AKT, but promote the protein expression of Bax, indicating that silencing SSRP1 can inhibit the proliferative capacity and increase the number of GC cells through incativating AKT signaling pathway. Conclusion: SSRP1 rose up in GC tissues and cells. Reduction of SSRP1 can inhibit the proliferative capacity and increase the number of GC cells through inactiving AKT signaling pathway.

scholarly journals The tRNA-derived fragment 5026a inhibits the proliferation of gastric cancer cells by regulating the PTEN/PI3K/AKT signaling pathway

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Linwen Zhu ◽  
Zhe Li ◽  
Xiuchong Yu ◽  
Yao Ruan ◽  
Yijing Shen ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Gastric Cancer Cells ◽  
Qrt Pcr

Abstract Background Recently, tRNA-derived fragments (tRFs) have been shown to serve important biological functions. However, the role of tRFs in gastric cancer has not been fully elucidated. This study aimed to identify the tumor suppressor role of tRF-5026a (tRF-18-79MP9P04) in gastric cancer. Methods Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was first used to detect tRF-5026a expression levels in gastric cancer tissues and patient plasma. Next, the relationship between tRF-5026a levels and clinicopathological features in gastric cancer patients was assessed. Cell lines with varying tRF-5026a levels were assessed by measuring tRF-5026a using qRT-PCR. After transfecting cell lines with a tRF-5026a mimic or inhibitor, cell proliferation, colony formation, migration, apoptosis, and cell cycle were evaluated. The expression levels of related proteins in the PTEN/PI3K/AKT pathway were also analyzed by Western blotting. Finally, the effect of tRF-5026a on tumor growth was tested using subcutaneous tumor models in nude mice. Results tRF-5026a was downregulated in gastric cancer patient tissues and plasma samples. tRF-5026a levels were closely related to tumor size, had a certain diagnostic value, and could be used to predict overall survival. tRF-5026a was also downregulated in gastric cancer cell lines. tRF-5026a inhibited the proliferation, migration, and cell cycle progression of gastric cancer cells by regulating the PTEN/PI3K/AKT signaling pathway. Animal experiments showed that upregulation of tRF-5026a effectively inhibited tumor growth. Conclusions tRF-5026a (tRF-18-79MP9P04) is a promising biomarker for gastric cancer diagnostics and has tumor suppressor effects mediated through the PTEN/PI3K/AKT signaling pathway.

scholarly journals Capicua homology protein inhibits the progression of gastric cancer through the PI3K/AKT signaling pathway

2020 ◽  
Author(s):  
LU GE ◽  
Chang-long Hu ◽  
Zheng-hui Ge ◽  
Chun-rong Wang ◽  
Li Qian ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Western Blot ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Epithelial Mesenchymal Transition ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Mesenchymal Transition ◽  
Matrigel Invasion ◽  
Qrt Pcr

Abstract Purpose Capicua homolog protein (CIC) played a broad role in the development of cancer in humans, however, its role in the progression of gastric cancer (GC) specifically has been unclear. This study aimed to explore the expression of CIC and its potential clinical value in patients with GC. Methods The CIC levels in GC tissues and cell lines were examined by quantitative real-time polymerase chain reaction (qRT-PCR). And the in-vitro effects of CIC expression in MGC-803 cells on their proliferation, invasion, and the progression of epithelial-mesenchymal transition were assessed by CCK-8 assays, Matrigel-invasion analysis, qRT-PCR and Western blot assays, separately. In addition, the effects of downregulation of CIC on the activation of PI3K/AKT signaling pathway were measured using Western-blot analysis. Results The results showed CIC levels were lower in GC tissues and GC cell lines, and these lower CIC levels were correlated with tumor differentiation, Helicobacter pylori infection, TNM stage, and patient survival. In addition, CIC overexpression could promote cell proliferation, invasion, and progression of epithelial-mesenchymal transition in MGC-803 cells. Notably, exotic expression of CIC inactivated the phosphoinositide 3-kinase/protein kinase B signaling pathway. Conclusions In conclusion, our finding suggested CIC could serve as a potential diagnostic and prognostic biomarker and a probable therapy target for GC.

scholarly journals MicroRNA-1269 promotes cell proliferation via the AKT signaling pathway by targeting RASSF9 in human gastric cancer

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Wen-Li Liu ◽  
Hu-xia Wang ◽  
Cheng-xin Shi ◽  
Fei-yu Shi ◽  
Ling-yu Zhao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Target Gene ◽  
Akt Signaling ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Akt Signaling Pathway ◽  
Qrt Pcr

Abstract Background MicroRNAs (miRNAs) play key roles in tumorigenesis and progression of gastric cancer (GC). miR-1269 has been reported to be upregulated in several cancers and plays a crucial role in carcinogenesis and cancer progression. However, the biological function of miR-1269 in human GC and its mechanism remain unclear and need to be further elucidated. Methods The expression of miR-1269 in GC tissues and cell lines was detected by quantitative real-time PCR (qRT-PCR). Target prediction programs (TargetScanHuman 7.2 and miRBase) and a dual-luciferase reporter assay were used to confirm that Ras-association domain family 9 (RASSF9) is a target gene of miR-1269. The expression of RASSF9 was measured by qRT-PCR and Western blotting in GC tissues. MTT and cell counting assays were used to explore the effect of miR-1269 on GC cell proliferation. The cell cycle and apoptosis were measured by flow cytometry. RASSF9 knockdown and overexpression were used to further verify the function of the target gene. Results We found that miR-1269 expression was upregulated in human GC tissues and cell lines. The overexpression of miR-1269 promoted GC cell proliferation and cell cycle G1-S transition and suppressed apoptosis. The inhibition of miR-1269 inhibited cell growth and G1-S transition and induced apoptosis. miR-1269 expression was inversely correlated with RASSF9 expression in GC tissues. RASSF9 was verified to be a direct target of miR-1269 by using a luciferase reporter assay. The overexpression of miR-1269 decreased RASSF9 expression at both the mRNA and protein levels, and the inhibition of miR-1269 increased RASSF9 expression. Importantly, silencing RASSF9 resulted in the same biological effects in GC cells as those induced by overexpression of miR-1269. Overexpression of RASSF9 reversed the effects of miR-1269 overexpression on GC cells. Both miR-1269 overexpression and RASSF9 silencing activated the AKT signaling pathway, which modulated cell cycle regulators (Cyclin D1 and CDK2). In contrast, inhibition of miR-1269 and RASSF9 overexpression inhibited the AKT signaling pathway. Moreover, miR-1269 and RASSF9 also regulated the Bax/Bcl-2 signaling pathway. Conclusions Our results demonstrate that miR-1269 promotes GC cell proliferation and cell cycle G1-S transition by activating the AKT signaling pathway and inhibiting cell apoptosis via regulation of the Bax/Bcl-2 signaling pathway by targeting RASSF9. Our findings indicate an oncogenic role of miR-1269 in GC pathogenesis and the potential use of miR-1269 in GC therapy.

scholarly journals Absent in melanoma 2 suppresses gastric cancer cell proliferation and migration via inactivation of AKT signaling pathway

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Dong Wang ◽  
Junwei Zou ◽  
Jun Dai ◽  
Zhengwu Cheng
Keyword(s):  
Gastric Cancer ◽  
Signaling Pathway ◽  
Cellular Proliferation ◽  
Akt Signaling ◽  
Tnm Staging ◽  
Akt Signaling Pathway ◽  
Akt Inhibitor ◽  
Migration Ability ◽  
And Migration ◽  
Proliferation And Migration

AbstractGastric cancer (GC) is the third leading cause of cancer-related mortality worldwide, and poses a great threat to public health. Absent in melanoma 2 (AIM2), a member of the pyrin-HIN family proteins, plays various roles across different types of cancers. However, the possible role of AIM2 in GC, as well as the underling mechanisms, are equivocal and need to be further explored. Herein, we identified that AIM2 expression was significantly down-regulated in GC tissues. Furthermore, loss of AIM2 was significantly associated with tumor size, lymph node metastasis (LNM) and tumor, node, metastases (TNM) staging, as well as poor prognosis in GC patients. Knockdown of AIM2 in GC cells significantly promoted cellular proliferation and migration, whereas AIM2 overexpression did the opposite. Mechanistically, we discovered that AIM2 regulates the AKT signaling pathway. In fact, the enhanced proliferation and migration ability induced by AIM2 knockdown was partially impaired in cells treated with the AKT inhibitor. Overall, our findings suggests that AIM2 is an independent prognostic marker and highlights a new entry point for targeting the AIM2/AKT signaling axis for GC treatment.

scholarly journals MicroRNA-559 restrains gastric cancer progression via activating AKT signaling pathway by targeting TRIM14

2020 ◽  
Author(s):  
Li Wei ◽  
Lu Zhang ◽  
Bo Zhang ◽  
Guanghui Wang ◽  
Lei Meng ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cell Growth ◽  
Signaling Pathway ◽  
Target Gene ◽  
Akt Signaling ◽  
Cell Multiplication ◽  
Akt Signaling Pathway ◽  
Qrt Pcr ◽  
Tissue Specimens

Abstract Background: MicroRNAs (miRNAs) act as pivotal functions in gastric cancer (GC) carcinogenesis and progression. MiR-559 has been defined as a potential cancer suppressor gene in a few cancers. Nevertheless, the biological effect of miR-559 in human GC and the underlying molecular mechanism still unclear and need to be further illuminated. Methods: Quantitative real-time PCR (qRT-PCR) was fulfilled for measuring the miR-559 expression level in GC. The dual-luciferase reporter was used to verify that tripartite motif-containing 14 (TRIM14) is a target gene of miR-559. The expression levels of TRIM14 were examined by qRT-PCR and Western blot in GC tissue specimens and cell lines. The effects of miR-559 on GC cell growth were detected with MTT and cell counting assays. Cell cycle and apoptosis were examined by using flow cytometry. Overexpression and siRNA further demonstrated the role of TRIM14 in GC. Results: Our results revealed that miR-559 expression was dramatically downregulated in human GC tissue specimens and cell lines. MiR-559 overexpression restrained GC cell growth, and induced cell cycle G1-S phase arrest and apoptosis. MiR-559 inhibitors promoted cell multiplication and cell cycle G1-S transition, and inhibited apoptosis. MiR-559 level was negatively related to TRIM14 mRNA level in GC. The results showed that TRIM14 was affirmed to be a target gene of miR-559. MiR-559 overexpression downregulated the TRIM14 expression, and miR-559 inhibitors upregulated the TRIM14 expression. Particularly, knockdown of TRIM14 gave rise to the semblable cellular effects observed upon miR-559 overexpression. TRIM14 overexpression recapitulated the revulsive cellular and molecular effects by suppression of miR-559. Furthermore, both miR-559 overexpression and TRIM14 silencing led to the inhibition of the AKT signaling pathway. On the contrary, miR-559 suppression and TRIM14 overexpression activated the AKT signaling pathway, and inhibited Bax/Bcl-2 pathway. Conclusions: The findings illustrate that miR-559 restrains cell multiplication via suppressing the AKT signaling pathway in human GC and induces cell apoptosis through the suppression of Bax/Bcl-2 signaling pathway via targeting TRIM14. The findings imply that miR-559 acts as a pivotal function in human GC and represents a latent novel target in GC therapy.

scholarly journals COL6A3 promotes cellular malignancy of osteosarcoma by activating the PI3K/AKT pathway

2020 ◽  
Vol 66 (6) ◽  
pp. 740-745
Author(s):  
Hong-Li Guo ◽  
Gang Chen ◽  
Ze-Long Song ◽  
Jia Sun ◽  
Xi-Hai Gao ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Colony Formation ◽  
Akt Signaling ◽  
Cell Counting ◽  
Akt Pathway ◽  
Akt Signaling Pathway ◽  
Invasion And Migration ◽  
Geo Dataset ◽  
And Migration

SUMMARY OBJECTIVE In this study, we aimed to investigate the role of COL6A3 on cell motility and the PI3K/AKT signaling pathway in osteosarcoma. METHODS The relative expression of COL6A3 was achieved from a GEO dataset in osteosarcoma tissue. siRNA technology was applied to decrease the COL6A3 expression in cells, and cell counting kit-8 (CCK-8) assay and colony formation analysis were used to examine the cell proliferation potential. Knockdown COL6A3 made the proliferation and colony formation abilities worse than the COL6A3 without interference. Likewise, in contrast to the si-con group, cell invasion and migration were inhibited in the si-COL6A3 group. Moreover, the western blot results suggested that the PI3K/AKT signaling pathway was manipulated by measuring the protein expression of the PI3K/AKT pathway-related markers, due to the COL6A3 inhibition. CONCLUSION COL6A3 plays a crucial role in modulating various aspects of the progression of osteosarcoma, which would provide a potentially effective treatment for osteosarcoma.

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