scholarly journals The inhibitory role of miR‑485‑5p in colorectal cancer proliferation and invasion via targeting of CD147

2018 ◽  
Author(s):  
Yuqin Pan ◽  
Huiling Sun ◽  
Xiuxiu Hu ◽  
Bangshun He ◽  
Xiangxiang Liu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Proliferation ◽  
Inhibitory Role ◽  
Proliferation And Invasion

scholarly journals Oncogenic lncRNA ZNF561-AS1 is essential for colorectal cancer proliferation and survival through regulation of miR-26a-3p/miR-128-5p-SRSF6 axis

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Zizhen Si ◽  
Lei Yu ◽  
Haoyu Jing ◽  
Lun Wu ◽  
Xidi Wang
Keyword(s):  
Colorectal Cancer ◽  
Rna Binding ◽  
Xenograft Model ◽  
Luciferase Reporter ◽  
Cancer Proliferation ◽  
Mouse Xenograft ◽  
Mouse Xenograft Model

Abstract Background Long non-coding RNAs (lncRNA) are reported to influence colorectal cancer (CRC) progression. Currently, the functions of the lncRNA ZNF561 antisense RNA 1 (ZNF561-AS1) in CRC are unknown. Methods ZNF561-AS1 and SRSF6 expression in CRC patient samples and CRC cell lines was evaluated through TCGA database analysis, western blot along with real-time PCR. SRSF6 expression in CRC cells was also examined upon ZNF561-AS1 depletion or overexpression. Interaction between miR-26a-3p, miR-128-5p, ZNF561-AS1, and SRSF6 was examined by dual luciferase reporter assay, as well as RNA binding protein immunoprecipitation (RIP) assay. Small interfering RNA (siRNA) mediated knockdown experiments were performed to assess the role of ZNF561-AS1 and SRSF6 in the proliferative actives and apoptosis rate of CRC cells. A mouse xenograft model was employed to assess tumor growth upon ZNF561-AS1 knockdown and SRSF6 rescue. Results We find that ZNF561-AS1 and SRSF6 were upregulated in CRC patient tissues. ZNF561-AS1 expression was reduced in tissues from treated CRC patients but upregulated in CRC tissues from relapsed patients. SRSF6 expression was suppressed and enhanced by ZNF561-AS1 depletion and overexpression, respectively. Mechanistically, ZNF561-AS1 regulated SRSF6 expression by sponging miR-26a-3p and miR-128-5p. ZNF561-AS1-miR-26a-3p/miR-128-5p-SRSF6 axis was required for CRC proliferation and survival. ZNF561-AS1 knockdown suppressed CRC cell proliferation and triggered apoptosis. ZNF561-AS1 depletion suppressed the growth of tumors in a model of a nude mouse xenograft. Similar observations were made upon SRSF6 depletion. SRSF6 overexpression reversed the inhibitory activities of ZNF561-AS1 in vivo, as well as in vitro. Conclusion In summary, we find that ZNF561-AS1 promotes CRC progression via the miR-26a-3p/miR-128-5p-SRSF6 axis. This study reveals new perspectives into the role of ZNF561-AS1 in CRC.

scholarly journals miR-125 inhibits colorectal cancer proliferation and invasion by targeting TAZ

2019 ◽  
Vol 39 (12) ◽  
Author(s):  
Meiyuan Yang ◽  
Xiaoli Tang ◽  
Zheng Wang ◽  
Xiaoqing Wu ◽  
Dong Tang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Underlying Mechanism ◽  
Cell Counting ◽  
Binding Motif ◽  
Cancer Proliferation ◽  
Qrt Pcr ◽  
Sirna Knockdown ◽  
Proliferation And Invasion ◽  
Hct116 Cells

Abstract Colorectal cancer (CRC) is the third most common malignant tumor worldwide and is a serious threat to human health. MicroRNAs (miRNAs) play a key role in oncogenesis and cancer progression. MiRNA-125 (miR-125) is an important miRNA that is dysregulated in several kinds of cancers. Thus, we investigated the expression and effects of miR-125 and Transcriptional co-activator with PDZ-binding motif (TAZ) for a better understanding of the underlying mechanism of tumor progression in CRC, which may provide an emerging biomarker for diagnosis and treatment of CRC. We measured the expression levels of miR-125 in CRC tissues, adjacent tissues, and cell lines (e.g. HCT116, SW480, FHC) by quantitative real-time polymerase chain reaction (qRT-PCR). The effect of miR-125 on proliferation and invasion in CRC cells was detected by Cell Counting Kit-8 (CCK-8), clone formation assay, and transwell assay. Western blotting and qRT-PCR were used to investigate the expression of TAZ after knocking down miR-125 in HCT116 cells or overexpressing miR-125 in SW480 cells. MiR-125 was significantly down-regulated in CRC compared with pericarcinomatous tissue from 18 patients. An miR-125 inhibitor promoted CRC cell proliferation and invasion, while miR-125 mimic had the opposite effect. Moreover, we found that TAZ was an miR-125 target and the siRNA knockdown of TAZ could reverse the effect of the miR-125 inhibitor on proliferation and invasion in HCT116 cells. The present study shows that miR-125 suppresses CRC proliferation and invasion by targeting TAZ.

scholarly journals TGF-β1 induces HMGA1 expression: The role of HMGA1 in thyroid cancer proliferation and invasion

2017 ◽  
Vol 50 (5) ◽  
pp. 1567-1578 ◽  
Author(s):  
Jing Zhong ◽  
Chang Liu ◽  
Qing Hai Zhang ◽  
Ling Chen ◽  
Ying-Ying Shen ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cancer Proliferation ◽  
Hmga1 Expression ◽  
Proliferation And Invasion ◽  
Tgf Β1

scholarly journals Knockdown of SPOCK1 Inhibits the Proliferation and Invasion in Colorectal Cancer Cells by Suppressing the PI3K/Akt Pathway

2016 ◽  
Vol 24 (6) ◽  
pp. 437-445 ◽  
Author(s):  
Ping Zhao ◽  
Hai-Tao Guan ◽  
Zhi-Jun Dai ◽  
Yu-Guang Ma ◽  
Xiao-Xu Liu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Potential Therapeutic Target ◽  
Colorectal Cancer Cells ◽  
First Time ◽  
Proliferation In Vitro ◽  
Proliferation And Invasion ◽  
Hct116 Cells

Sparc/osteonectin, cwcv, and kazal-like domains proteoglycan (testican) 1 (SPOCK1), known as testican-1, were found to be involved in the development and progression of tumors. However, in colorectal cancer (CRC), the expression pattern of SPOCK1 and its functional role remain poorly investigated. In the present study, we explored the role of SPOCK1 in CRC. Our results demonstrated that SPOCK1 is overexpressed in CRC cell lines. SPOCK1 silencing significantly inhibited the proliferation in vitro and the tumor growth in vivo. Furthermore, SPOCK1 silencing significantly attenuated the migration/invasion by reversing the EMT process in CRC cells. Finally, knockdown of SPOCK1 obviously decreased the protein expression levels of p-PI3K and p-Akt in HCT116 cells. In total, our study demonstrated for the first time that knockdown of SPOCK1 inhibits the proliferation and invasion in CRC cells, possibly through the PI3K/Akt signaling pathway. Therefore, SPOCK1 may be a potential therapeutic target for the treatment of CRC.

Epigenetic silencing of NDRG2 promotes colorectal cancer proliferation and invasion

2015 ◽  
Vol 31 (1) ◽  
pp. 164-171 ◽  
Author(s):  
Sung Noh Hong ◽  
Sung Jin Kim ◽  
Eun-Ran Kim ◽  
Dong Kyung Chang ◽  
Young-Ho Kim
Keyword(s):  
Colorectal Cancer ◽  
Epigenetic Silencing ◽  
Cancer Proliferation ◽  
Proliferation And Invasion

scholarly journals N6-Methyladenosine Modification of PTTG3P Contributes to Colorectal Cancer Proliferation via YAP1

2021 ◽  
Vol 11 ◽  
Author(s):  
Yang Zheng ◽  
Yue Wang ◽  
Yiyang Liu ◽  
Longfei Xie ◽  
Jinnian Ge ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Expression Profiles ◽  
Critical Role ◽  
Methylation Status ◽  
Tumor Model ◽  
Loss Of Function ◽  
Cancer Proliferation ◽  
Mrna Binding

BackgroundLong noncoding RNAs (lncRNAs) have emerged to have irreplaceable roles in the epigenetic regulation of cancer progression, but their biological functions in colorectal cancer (CRC) remain unclear.MethodsLncRNA expression profiles in CRC tissue and their normal counterpart were explored. Through gain and loss of function approaches, the role of lncRNA PTTG3P was validated in relevant CRC cells and subcutaneous tumor model. The correlations of PTTG3P expression with clinical outcomes were assessed.ResultsPTTG3P was upregulated in CRC tissues and was closely correlated with unsatisfactory prognosis. PTTG3P facilitated glycolysis and proliferation, and the transcriptional regulator YAP1 was necessary for PTTG3P-induced proliferation. Mechanistically, the N6-methyladenosine (m6A) subunit METTL3 increased PTTG3P expression by influencing its stability, while insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) could identify PTTG3P m6A methylation status and bind to it. IGF2BP2 knockdown partly recovered PTTG3P expression induced by METTL3, indicating that METTL3-regulated PTTG3P expression depended on the presence of IGF2BP2. Finally, rescue assays validated the critical role of the METTL3/PTTG3P/YAP1 axis on CRC proliferation.ConclusionsPTTG3P is an independent prognostic biomarker for CRC. The METTL3/PTTG3P/YAP1 axis promotes the progression of CRC and is a promising treatment target.

scholarly journals The Role of Mitochondrial Fat Oxidation in Cancer Cell Proliferation and Survival

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2600
Author(s):  
Matheus Pinto De Oliveira ◽  
Marc Liesa
Keyword(s):  
Oxidative Stress ◽  
Colorectal Cancer ◽  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
De Novo ◽  
Lipid Synthesis ◽  
Acid Synthesis ◽  
Acid Oxidation ◽  
Cancer Proliferation

Tumors remodel their metabolism to support anabolic processes needed for replication, as well as to survive nutrient scarcity and oxidative stress imposed by their changing environment. In most healthy tissues, the shift from anabolism to catabolism results in decreased glycolysis and elevated fatty acid oxidation (FAO). This change in the nutrient selected for oxidation is regulated by the glucose-fatty acid cycle, also known as the Randle cycle. Briefly, this cycle consists of a decrease in glycolysis caused by increased mitochondrial FAO in muscle as a result of elevated extracellular fatty acid availability. Closing the cycle, increased glycolysis in response to elevated extracellular glucose availability causes a decrease in mitochondrial FAO. This competition between glycolysis and FAO and its relationship with anabolism and catabolism is conserved in some cancers. Accordingly, decreasing glycolysis to lactate, even by diverting pyruvate to mitochondria, can stop proliferation. Moreover, colorectal cancer cells can effectively shift to FAO to survive both glucose restriction and increases in oxidative stress at the expense of decreasing anabolism. However, a subset of B-cell lymphomas and other cancers require a concurrent increase in mitochondrial FAO and glycolysis to support anabolism and proliferation, thus escaping the competing nature of the Randle cycle. How mitochondria are remodeled in these FAO-dependent lymphomas to preferably oxidize fat, while concurrently sustaining high glycolysis and increasing de novo fatty acid synthesis is unclear. Here, we review studies focusing on the role of mitochondrial FAO and mitochondrial-driven lipid synthesis in cancer proliferation and survival, specifically in colorectal cancer and lymphomas. We conclude that a specific metabolic liability of these FAO-dependent cancers could be a unique remodeling of mitochondrial function that licenses elevated FAO concurrent to high glycolysis and fatty acid synthesis. In addition, blocking this mitochondrial remodeling could selectively stop growth of tumors that shifted to mitochondrial FAO to survive oxidative stress and nutrient scarcity.

scholarly journals MicroRNA-320b promotes colorectal cancer proliferation and invasion by competing with its homologous microRNA-320a

2015 ◽  
Vol 356 (2) ◽  
pp. 669-675 ◽  
Author(s):  
Jiaojiao Zhou ◽  
Mengwen Zhang ◽  
Yanqing Huang ◽  
Lin Feng ◽  
Hailong Chen ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Proliferation ◽  
Proliferation And Invasion

scholarly journals MicroRNA-96-5p represses breast cancer proliferation and invasion through Wnt/β-catenin signaling via targeting CTNND1

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Xiao-hui Gao ◽  
Ya-li Zhang ◽  
Zhi-ye Zhang ◽  
Shuang-shuang Guo ◽  
Xiao-bing Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cyclin D1 ◽  
Cancer Proliferation ◽  
Invasive Capacity ◽  
Novel Target ◽  
Proliferation And Invasion

AbstractLow miR-96-5p expression is characteristic of many cancers but its role in breast cancer (BCa) remains poorly defined. Here, the role of miR-96-5p in BC development was assessed. We demonstrate that exogenously expressing miR-96-5p inhibits the proliferative, migratory and invasive capacity of BCa cells. Mechanistically, miR-96-5p in BCa cells was found to target and downregulate catenin delta 1 (CTNND1) leading to decreased β-catenin expression, a loss of WNT11 signaling, reduced cyclin D1 levels and lower MMP7 expression. Exogenously expressing CTNND1 alleviated these effects. In summary, we are the first to reveal that miR-96-5p inhibits the proliferative, invasive and migratory phenotypes of BCa cells the targeting of CTNND1 and subsequent Wnt/β-catenin signaling. These data highlight miR-96-5p as a novel target for BC treatment.

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