Effect of Targeting Leucine-Zipper-Like Transcription Regulator 1 Gene on Colon Cancer Cells

2021 ◽  
Vol 11 (8) ◽  
pp. 1588-1594
Author(s):  
Xuemin Song ◽  
Dongming Luo ◽  
Qian Zhong ◽  
Ke Wei ◽  
Yangyang Tang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Real Time ◽  
Real Time Pcr ◽  
Leucine Zipper ◽  
Clinicopathological Characteristics ◽  
Control Group ◽  
Sw620 Cell ◽  
Cancer Tissues ◽  
Proliferation And Invasion

LZTR1 is associated with several diseases, including liver cancer, childhood cancer, and schwannomas. However, LZTR1’s role in colon cancer and its mechanism of action have not been reported. The colon cancer tissues and adjacent tissues were collected to measure the expression of LZTR1 by Real time PCR. Colon cancer SW620 cell lines were cultured and randomly divided into control group and LZTR1 group followed by analysis of LZTR1 expression by real time PCR, cell proliferation by MTT assay, Caspase3 activity, Bcl-2 and Bax level by Real time PCR, cell invasion by Transwell chamber; NF-κB/VEGF expression by Western blot. LZTR1 expression was significantly reduced in colon cancer tissues compared to adjacent tissues (P <0.05) and negatively correlated with colon cancer TNM stage, tumor size, and lymph node metastasis, and positively associated with tumor differentiation (P <0.05). LZTR1 plasmid transfection into SW620 cells can significantly up-regulate LZTR1, inhibit tumor cell proliferation and invasion, increase Caspase 3 activity and Bax level, downregulate Bcl-2, NF-κB and VEGF (P <0.05). LZTR1 expression is reduced in colon cancer tissues, which is related to its clinicopathological characteristics. Up-regulation of LZTR1 can regulate apoptosis and inhibit tumor proliferation and invasion by regulating NF-κB/VEGF signaling pathway.

The Regulatory Effect of Mir-149 on Bone Marrow Mesenchymal Stem Cells in Osteoporosis Rats and Its Related Mechanisms

2019 ◽  
Vol 9 (8) ◽  
pp. 1127-1132 ◽  
Author(s):  
Long Wang ◽  
Jian Yu
Keyword(s):  
Cell Proliferation ◽  
Real Time ◽  
Real Time Pcr ◽  
Mapk Signaling ◽  
Control Group ◽  
Regulatory Effect ◽  
Erk Mapk ◽  
Alp Activity ◽  
Sd Rats ◽  
Marrow Mesenchymal Stem Cells

BMSCs play an important role in osteoporosis (OP) and their differentiation can lead to OP progression. Mir-149 can participate in the regulation of BMSCs. However, the effect of Mir-149 on BMSCs in osteoporosis remains unclear. SD rats were divided control group and OP group. OP rat BMSCs were transfected with Mir-149 siRNA followed by analysis of Mir-149 expression by real time PCR, cell proliferation by MTT assay, apoptosis by flow cytometry, ERK/MAPK signaling protein expression by western blot, ALP activity, as well as expression of osteogenic genes Runx2 and OC by real time PCR. Mir-149 expression was significantly increased in BMSCs of OP rats, cell proliferation was inhibited, apoptosis was increased, as well as p-ERK1/2 expression, ALP activity and expression of Runx2 and OC was decreased compared to control group (P < 0.05). Transfection of Mir-149 siRNA into OP rat BMSCs reduced Mir-149 expression, promoted cell proliferation, decreased apoptotic rate, increased p-ERK1/2 expression, ALP activity and Runx2 and OC expression. Compared with OP group, the differences were statistically significant (P< 0.05). Mir-149 expression was increased in OP rat BMSCs. Down-regulation of Mir-149 promoted the activation of ERK/MAPK signaling pathway, inhibited apoptosis of BMSCs and promoted the proliferation and osteogenic differentiation of BMSCs in OP rats.

Long Non-Coding RNA Small Nucleolar RNA Host Gene 15 (SNHG15) Regulates Gastric Cancer Cell Proliferation and Invasion Through Targeting MiR-92a

2020 ◽  
Vol 10 (4) ◽  
pp. 518-524
Author(s):  
Feng Deng ◽  
Xiaoping Zhou ◽  
Yang Liu ◽  
Haiding Wang ◽  
Yinzi Li
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Real Time ◽  
Cancer Cell ◽  
Real Time Pcr ◽  
Gastric Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Pathological Stage ◽  
Gastric Cancer Cell Proliferation ◽  
Proliferation And Invasion

Gastric cancer pathogenesis remains to be elucidated. LncRNAs involve in tumorigenesis. LncRNA SNHG15 is abnormally expressed in several tumors, but its role in gastric cancer is unclear. The tumor tissue and adjacent tissues of gastric cancer patients were collected for measuring LncRNA SNHG15 and miR-92a expressions by Real time PCR. Gastric cancer cell line SGC-7901 was divided into NC group, si-SNHG15 group, and si-UCA1+ miR-92a inhibitor group followed by analysis of cell proliferation by MTT assay, Capase-3 activity as well as Bax and Bcl-2 level by Real-time PCR. Gastric cancer tissues presented significantly increased LncRNA SNHG15 and decreased miR-92a expression than adjacent tissues (P < 0 05). LncRNA SNHG15 and miR-92a expression was associated with the tumor differentiation and pathological stage (P < 0 05) with a negative correlation between them. SNHG15 siRNA transfection significantly inhibited SNHG15 expression and tumor cell proliferation and invasion, increased Caspase 3 activity and Bax level, and decreased Bcl2 (P < 0 05). miR-92a was a targeted miRNA for LncRNA SNHG15. Addition of miR-92a inhibitor can significantly reverse the above changes (P < 0 05). LncRNA SNHG15 expression is increased and miR-92a expression is decreased in gastric cancer and correlated with the tumor pathological stage. LncRNA SNHG15 regulates human gastric cancer cell proliferation, apoptosis and invasion via targeting miR-92a.

miR-34 Promotes Autophagy and Apoptosis of Spinal Chondrocytes by Mammalian Target of Rapamycin/Phosphatidylinositol-3-Kinase/Protein Kinase B Signaling

2020 ◽  
Vol 10 (12) ◽  
pp. 1877-1883
Author(s):  
Jun Wu ◽  
Fenfen Zhao ◽  
Feng Tian ◽  
Feng Ma ◽  
Tao Guan
Keyword(s):  
Cell Proliferation ◽  
Real Time ◽  
Signaling Pathway ◽  
Real Time Pcr ◽  
Caspase 3 ◽  
Akt Signaling ◽  
Chondrocyte Apoptosis ◽  
Control Group ◽  
Akt Signaling Pathway ◽  
Articular Chondrocyte

Autophagy and apoptosis of chondrocytes participate in spondyloarthritis (SpA). miR-34 involves in various diseases. However, miR-34’s role in autophagy and apoptosis of spine chondrocytes remains unclear. SpA patients and normal bone and articular cartilage tissues were collected, and miR-34 level was detected by Real-time PCR. The chondrocytes of SpA patients were isolated and divided into control group, miR-34 siRNA group and miR-34 group followed by analysis of Caspase 3 activity, cell proliferation by MTT assay, expression of Bax, Bcl-2, ATG5 and Beclin1 by Real time PCR, mTOR/PI3K/AKT signaling pathway protein expression by western blot, as well as TNF-α and IL-6 secretion by ELISA. miR-34 was significantly upregulated in SpA patients compared to normal (P <0.05). miR-34 siRNA transfection into SpA chondrocytes significantly down-regulated miR-34 expression, promoted cell proliferation, decreased Caspase 3 activity and Bax expression, increased Bcl-2, ATG5 and Beclin1 expression, decreased TNF-α and IL- 6 secretion as well as increased pmTOR and pAKT expression (P <0.05). miR-34 mimics was transfected into SpA chondrocytes, which up-regulated miR-34 expression and significantly reversed the above changes (P <0.05). miR-34 is upregulated in SpA patients. Down-regulation of miR-34 inhibits articular chondrocyte apoptosis and promotes autophagy by down-regulatingmTOR/PI3K/AKT signaling pathway, thereby promoting articular chondrocyte proliferation and inhibiting joint inflammation.

Long Noncoding RNA Myocardial Infarction-Associated Transcript as a Cancer Promoting Factor in Colon Cancer Development

2019 ◽  
Vol 9 (5) ◽  
pp. 655-661
Author(s):  
Wang Zhi ◽  
Jiang Zongdan ◽  
Zhang Yushu ◽  
Xu Xiaojun ◽  
Zhang Zhenyu
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Wound Healing ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Cell Number ◽  
Cyclin D3 ◽  
Sw620 Cell ◽  
Invasion And Migration ◽  
Cancer Tissues

Objection: The study aimed to explain the effects and mechanisms of long noncoding RNA (lncRNA) MIAT in development of colon cancer. Methods: The adjacent and cancer tissues which were collected from 30 cases colon cancer patients were evaluated pathology by HE staining and lncRNA MIAT expression by ISH assay. In the vitro study, SW620 cells were divided into NC, siRNA-control and siMIAT groups. Measuring cell proliferation, apoptosis, cell cycle, invasion and migration by CCK-8, flow cytometry, transwell and wound healing, and evaluating the relative proteins expressions by WB assay. Results: Compared with adjacent normal tissues, the lncRNA MIAT was significantly up-regulation in colon cancer tissues (P < 0.001). By cell experiment, with lncRNA MIAT knockdown, the cell proliferation was significantly depressed (P < 0.001) via significantly improving cell apoptosis and keeping the cell in the G1 phase (P < 0.001, respectively); the invasion SW620 cell number and wound healing rate were significantly suppressed (P < 0.001, respectively). The relative proteins (CDK2, Cyclin D3 and MMP-9) expressions of siMIAT group were significantly down-regulation compared with those of NC group (P < 0.001, respectively). Conclusion: Our study found that lncRNA MIAT expression is closely associated with colon cancer and may be one of key roles in progression and metastasis in colon cancer.

Effect of Long-Chain Non-Coding RNA GAS5 on Osteogenic/Adipogenic Differentiation of Bone Marrow Mesenchymal Stem Cells Under Oxidative Stress Through Targeting MiR-365

2019 ◽  
Vol 9 (12) ◽  
pp. 1751-1757
Author(s):  
Wenming Wu ◽  
Dongming Liang
Keyword(s):  
Oxidative Stress ◽  
Cell Proliferation ◽  
Real Time ◽  
Real Time Pcr ◽  
Adipogenic Differentiation ◽  
Control Group ◽  
Sod Activity ◽  
Stress Group ◽  
Alp Activity ◽  
Lncrna Gas5

Oxidative stress affects BMSCs. LncRNA GAS5 regulates cell proliferation and apoptosis. However, the effect of LncRNA GAS5 on osteogenesis/adipogenic differentiation of BMSCs under oxidative stress has not been reported. Rat BMSCs were cultured and randomly divided into 4 groups, normal control group; oxidative stress group; GAS5 siRNA group; GAS5 siRNA+ miR-365 inhibitor group followed by analysis of LncRNA GAS5 expression by Real time PCR, cell proliferation by MTT assay, Caspase3 activity, GAS5 and miR-365 targeting relationship by luciferase reporter assay, ALP activity, expression of Runx2, OP and PPAR 2 by Real time PCR, as well as ROS content and SOD activity. In oxidative stress group, GAS5 expression was significantly increased along with inhibited cell proliferation, increased Caspase3 activity, decreased ALP activity and the expression of Runx2 and OP, increased PPAR 2 expression and ROS content, and decreased SOD activity compared to control group (P < 0 05). miR-365 was the target miRNA of GAS5. GAS5 siRNA down-regulated GAS5 expression, significantly promoted cell proliferation, inhibited Caspase3 activity, increased ALP activity and Runx2 and OP expression, decreased PPAR 2 expression and ROS content, and increased SOD activity. (P < 0 05). However, GAS5 siRNA+ miR-365 inhibitor group reversed the effect of GAS5 siRNA. Oxidative stress promotes LncRNA GAS5 expression in BMSCs. LncRNA GAS5 regulates oxidative stress by targeting miR-365. Knockdown of GAS5 can promote BMSCs proliferation and osteogenic differentiation and inhibit adipogenic differentiation under oxidative stress.

Overexpression of Heme Oxygenase-1 Promotes Osteoblast Differentiation of Osteoporosis Rat Bone Marrow Stromal Cells in Bone Morphogenetic Protein-Dependent Manner

2019 ◽  
Vol 9 (11) ◽  
pp. 1614-1620
Author(s):  
Jiangrong Fan ◽  
Yong Zheng ◽  
Jingyang You
Keyword(s):  
Cell Proliferation ◽  
Real Time ◽  
Heme Oxygenase ◽  
Real Time Pcr ◽  
Osteoblast Differentiation ◽  
Caspase 3 ◽  
Control Group ◽  
Heme Oxygenase 1 ◽  
Dependent Manner ◽  
Alp Activity

BMSCs play a role in osteoporosis (OP) and their differentiation can lead to OP progression. Heme oxygenase-1 (HO-1) involves in many diseases, but the effect of HO-1 on osteoblast differentiation of BMSCs in OP rats remains unclear. SD rats were divided into control group and OP group. Rats BMSCs in OP group were cultured in vitro, HO-1 expression was up-regulated by HO-1 agonist hemin, and BMPR inhibitor LDN-19318 was added followed by analysis of HO-1 expression by real time PCR and ELISA, cell proliferation by MTT assay, apoptosis by Caspase 3 activity, BMP-2 expression by Western blot, ALP activity, expression of Runx2 and OC by real time PCR. In OP group, HO-1 expression was significantly decreased, cell proliferation was inhibited, Caspase 3 activity was increased along with decreased ALP activity and expression of Runx2, OC and BMP-2 compared to control (P < 0.05). Up-regulation of HO-1 expression significantly promoted cell proliferation, reduced Caspase 3 activity, increased ALP activity, and expression of Runx2, OC and BMP-2 (P < 0.05). However, inhibition of HO-1 significantly promoted bone differentiation after the addition of BMPR inhibitor LDN-193189 (P < 0.05). HO-1 expression is decreased in BMSCs of OP group rats. Up-regulation of HO-1 promoted BMSCs proliferation in OP rats in BMP-dependent manner, inhibited apoptosis, and promoted osteoblast differentiation.

scholarly journals MiR-6803-5p Promotes Cancer Cell Proliferation and Invasion via PTPRO/NF-κB Axis in Colorectal Cancer

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Shushan Yan ◽  
Min Cheng ◽  
Quanhong Duan ◽  
Zengfang Wang ◽  
Wenfeng Gao ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Real Time ◽  
Cancer Cell ◽  
Real Time Pcr ◽  
Mononuclear Cells ◽  
Colorectal Carcinogenesis ◽  
Luciferase Reporter ◽  
Cancer Cell Proliferation ◽  
Proliferation And Invasion

Accumulated studies have implicated microRNAs (miRNAs) exert modifying effects on colorectal cancer (CRC). Protein tyrosine phosphatase, receptor type O (PTPRO) has been identified as a tumor suppressor in several kinds of cancer, including CRC. Previously, we have found that exosome-encapsulated miR-6803-5p is increased in CRC. However, the mechanism of miR-6803-5p in CRC is not clear yet. This study is aimed at elucidating the effect of miR-6803-5p in colorectal carcinogenesis. Expression of miR-6803-5p and PTPRO mRNA in peripheral blood mononuclear cells of CRC patients is estimated by real-time PCR. PTPRO protein in CRC cells is detected by western blot. To verify the association of miR-6803-5p with PTPRO, luciferase reporter assay is performed. CCK-8 and EdU assays are conducted to assess cell proliferation. Real-time PCR and ELISA are applied to detect cytokine expression in CRC cells. Cell invasion and migration assays are evaluated by transwell and scratch tests. Immunofluorescence is carried out to determine the activation of NF-κB in HCT116 cells. Negative correlation is demonstrated between miR-6803-5p and PTPRO in CRC. PTPRO is demonstrated to be a direct target of miR-6803-5p. miR-6803-5p can promote cancer cell proliferation and invasion and enhance inflammation through PTPRO/NF-κB axis in CRC, which serves as a useful target for CRC.

scholarly journals Down-regulation LncRNA-SNHG15 contributes to proliferation and invasion of bladder cancer cells

BMC Urology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Aldhabi Mokhtar ◽  
Chuize Kong ◽  
Zhe Zhang ◽  
Yan Du
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Tumor Stage ◽  
Rt Pcr ◽  
Down Regulation ◽  
Bladder Cancer Cells ◽  
Cancer Tissues ◽  
Proliferation And Invasion

Abstract Objectives The aim of this study was to investigate the effect of lncRNA-SNHG15 in bladder carcinoma using cell lines experiments and the relationship between clinical characteristics and lncRNA-SNHG15 expression was analyzed. Methods Bladder cancer tissues and near-cancer tissues were collected. The real-time PCR (RT-PCR) was used to detect the expression of lncRNA-SNHG15 in tissues and cell lines. The expression of lncRNA-SNHG15 was downregulated by interference (siRNA), as detected by RT-PCR, that was used to determine the efficiency of the interference. CCK-8 and Transwell assays were used to evaluate the effect of lncRNA-SNHG15 on the proliferation and invasion capability of bladder cancer cells. The t-test was used for Statistical analyses, which were carried out using the Statistical Graph pad 8.0.1.224 software. Result The expression of lncRNA-SNHG15 was up regulated in 5637, UMUC3 and T24 cell lines compared with corresponding normal controls (P < 0.05). Up regulation was positively related to tumor stage (P = 0.015). And tumor size (P = 0.0465). The down-regulation of lncRNA-SNHG15 with siRNA significantly inhibited UMUC3 and T24 cell proliferation and invasion. Conclusion This study showed that lncRNA-SNHG15 is overexpressed in bladder cancer tissues and (5637, UMUC3 T24) cell lines. Up regulation was positively related to tumor stage (P = 0.015), and tumor size (P = 0.0465). Down-regulation of lncRNA-SNHG15 by siRNA significantly inhibited UMUC3 and T24 cell proliferation and invasion, indicating a potential molecular target for future tumor targeted therapy.

scholarly journals Enhanced intestinal epithelial cell proliferation in diabetic rats correlates with β-catenin accumulation

2015 ◽  
Vol 226 (3) ◽  
pp. 135-143 ◽  
Author(s):  
Tatiana Dorfman ◽  
Yulia Pollak ◽  
Rima Sohotnik ◽  
Arnold G Coran ◽  
Jacob Bejar ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Real Time ◽  
Real Time Pcr ◽  
Intestinal Epithelial Cell ◽  
Diabetic Rats ◽  
Male Rats ◽  
Intestinal Cell ◽  
Intestinal Epithelial ◽  
Epithelial Cell Proliferation

The Wnt/β-catenin signaling cascade is implicated in the control of stem cell activity, cell proliferation, and cell survival of the gastrointestinal epithelium. Recent evidence indicates that the Wnt/β-catenin pathway is activated under diabetic conditions. The purpose of this study was to evaluate the role of Wnt/β-catenin signaling during diabetes-induced enteropathy in a rat model. Male rats were divided into three groups: control rats received injections of vehicle; diabetic rats received injections of one dose of streptozotocin (STZ); and diabetic–insulin rats received injections of STZ and were treated with insulin given subcutaneously at a dose of 1 U/kg twice daily. Rats were killed on day 7. Wnt/β-catenin-related genes and expression of proteins was determined using real-time PCR, western blotting, and immunohistochemistry. Among 13 genes identified by real-time PCR, seven genes were upregulated in diabetic rats compared with control animals including the target genes c-Myc and Tcf4. Diabetic rats also showed a significant increase in β-catenin protein compared with control animals. Treatment of diabetic rats attenuated the stimulating effect of diabetes on intestinal cell proliferation and Wnt/β-catenin signaling. In conclusion, enhanced intestinal epithelial cell proliferation in diabetic rats correlates with β-catenin accumulation.

Effects of LncRNA HOX Transcript Antisense RNA Targeting miRNA-761 on Cervical Cancer Cell Proliferation and Apoptosis

2021 ◽  
Vol 11 (10) ◽  
pp. 2081-2086
Author(s):  
Bin Qiu ◽  
Hui Zhong ◽  
Shenqiu Ming ◽  
Chunxia Zhu
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Control Group ◽  
Normal Tissues ◽  
Cell Clones ◽  
Cervical Cancer Cells ◽  
Set Up ◽  
Cancer Tissues ◽  
Lncrna Hotair

Abnormal LncRNA HOTAIR level is correlated with various cancers and miR-761 can inhibit cancers. LncRNA HOTAIR targets miR-761 by StarBase 2.0 analysis. Our study investigated whether LncRNA HOTAIR can affect cervical cancer cells by regulating miR-761. The control group (NC group), LncRNA HOTAIR group and LncRNA HOTAIR + miR-761 Mimics group were set up to measure LncRNA HOTAIR and miR-761 level by qRT-PCR. Dual fluorescein reporter assay assessed whether miR-761 binds LncRNA HOTAIR. Western blot was used to measure Cyclin D1, Bcl-2 and Tubulin expression and clone formation assay was to assess cell proliferation and Annexin VFITC/PI staining was to detect cell apoptosis. Compared with normal tissues, LncRNA HOTAIR level was significantly higher in cervical cancer tissues, while miR-761 was lower (P < 0.01). LncRNA HOTAIR targets miR-761. Compared with NC group, CyclinD1 and Bcl-2 in LncRNA HOTAIR group were significantly increased (P < 0.01), which were significantly lower in LncRNA HOTAIR + miR-761 Mimics group (P < 0.05). Compared to NC group, miR-761 in LncRNA HOTAIR group was significantly reduced (P < 0.01) and elevated by miR-761 Mimics. In addition, compared to NC group, the number of cell clones in LncRNA HOTAIR group was increased, cell proliferation was increased, and number of apoptotic cells was decreased, which were all reversed in the LncRNA HOTAIR + miR-761 Mimics group. LncRNA HOTAIR targets miR-761, promotes cell proliferation and reduces cell apoptosis. miR-761 mimics can partially prevent the effects of LncRNA HOTAIR.

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