The Novel Role of Arsenic (+3 oxidation state) Methyltransferase in Arsenic Genotoxicity

Abstract Background: Arsenic (+3 oxidation state) methyltransferase (AS3MT) is the key enzyme in methylation metabolism of arsenic. It is closely related to DNA methylation, but little is known about the novel molecular mechanisms.Methods: 79 workers and 41 individuals in the control group were recruited. Arsenic, relative indexes, 28 relative RNAs, and base modifications of exon 5-8 of p53 were detected. Enzyme linked immunosorbent assay(ELISA) was performed to detect the expression of AS3MT protein in all subjects. A series of methods were used to analyze the relationships between them. The AS3MT protein was detected in A549 and 16HBE cells after treated using sodium arsenite, MMA and DMA for 48 hours. Small interfering RNA (siRNA) transfection was used to investigate the role of AS3MT in arsenite-induced tumorigenesis. The cell proliferation and apoptosis were assessed with MTT assay, EdU assay, HO/PI double staining and JC-1 assay. The real-time quantitative PCR (qRT-PCR) and Western Blot analyses were used to evaluate the expression of genes. The p53 luciferase reporter gene assay and Co-immunoprecipitation (Co-IP) were used to identify the interactions of target proteins.Results: AS3MT RNA is closely related to p53, a series of ncRNAs and mRNAs, and likely to have causal correlations. Base modifications of p53, miR-548 and miR-190 have significant distinctive effects, but arsenic may play limited roles. AS3MT is over expression in lung cancer patients who have not exposed to arsenic, human lung adenocarcinoma and bronchial epithelial cells with arsenic treatment for 48h. AS3MT protein is induced in arsenic exposed population. Down regulation of AS3MT inhibit proliferation and promotes apoptosis of cells. Mechanistically, AS3MT specifically bind with c-Fos, and block the binding ability between c-Fos and c-Jun. Additionally, knockdown of AS3MT mediated by siRNA enhance the phosphorylation level of p53 Ser392 through activating p38 MAPK. These probably lead to activation of p53 signaling and up regulation in downstream targets, such as p21, Fas, Puma and Bax.Discussion: Here showed that AS3MT RNA plays a great role in the genotoxicity and carcinogenesis which started by arsenic, but influenced by other factors. Up regulation of AS3MT can directly act on cell, and affect cell proliferation and apoptosis through activation of p53 signaling and up regulation in downstream targets.

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PITPNA-AS1 Activated by H3K27ac Sponged miR-98-5p to Regulate Cisplatin Resistance in Gastric Cancer

10.21203/rs.3.rs-156344/v1 ◽

2021 ◽

Author(s):

Yaping Liu ◽

Xu Zhao ◽

Yinnan Chen ◽

Gang Guo ◽

Jiansheng Wang ◽

...

Keyword(s):

Gastric Cancer ◽

Cell Proliferation ◽

Molecular Mechanisms ◽

Luciferase Reporter ◽

Platinum Resistance ◽

Luciferase Reporter Gene ◽

Gene Assay ◽

Proliferation And Apoptosis ◽

Gastric Cancer Cell Lines ◽

Cancer Tissues

Abstract To evaluate the expression of PITPNA-AS1 and miR-98-5p in gastric cancer tissues as well as their association with progression of gastric cancer, and investigate the role of PITPNA-AS1 and miR-98-5p in developing platinum resistance. RNA sequencing was used to identify candidate lncRNAs and microRNAs related to local recurrence of gastric cancer. qRT-PCR was used to investigate the expression of PITPNA-AS1 and miR-98-5p. CCK-8 and caspase3/7 activity were used to evaluate the cell proliferation and apoptosis rate. Dual luciferase reporter gene assay and RNA pull down were used to evaluate the cross talk between PITPNA-AS1 and miR-98-5p. PITPNA-AS1 and miR-98-5p could regulate cell proliferation and inhibit apoptosis in gastric cancer cell lines. Cisplatin and lobaplatin could significantly suppress the expression of PITPNA-AS1, which interacted with negatively regulated miR-98-5p expression. PITPNA-AS1 overexpression impaired the effect of platinum, which was partially reversed by downregulation of miR-98-5p knock down. In gastric cancer, PITPNA-AS1 and miR-98-5p could regulat cell growth, apoptosis and platinum resistance. They have the potential to be biomarkers and curative therapeutic targets. However, further research on molecular mechanisms are needed.

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miR-495-3p Depresses Cell Proliferation and Migration By Down-Regulating HMGB1 in Colorectal Cancer

10.21203/rs.3.rs-663678/v1 ◽

2021 ◽

Author(s):

Zhang Jieling ◽

Li Kai ◽

Zheng Huifen ◽

Zhu Yiping

Keyword(s):

Colorectal Cancer ◽

Cell Proliferation ◽

Luciferase Reporter ◽

Luciferase Reporter Gene ◽

Gene Assay ◽

And Migration ◽

Cancer Tissues

Abstract Background: MicroRNAs play an important role in the genesis and progression of tumors, including colorectal cancer (CRC), which has a high morbidity and mortality rate. In this research, the role of miR-495-3p and HMGB1 in CRC was investigated.Methods: We performed qRT-PCR to detect the expression of miR-495-3p in colorectal cancer tissues and cell lines. Functional experiments such as CCK-8 assay, EDU assay, Transwell assay and apoptosis assay were conducted to explore the effects of miR-495-3p on the proliferation, migration and apoptosis of CRC cells in vitro. Then, the use of database prediction, dual-luciferase reporter gene assay and functional experiments verified the role of miR-495-3p target gene HMGB1 in CRC. Finally, rescue experiments was performed to investigate whether overexpression of HMGB1 could reverse the inhibitory effect of miR-495-3p on CRC cell proliferation in vivo and in vitro.Results: miR-495-3p was down-regulated in colorectal cancer tissues and cell lines, and could inhibit the proliferation and migration of colorectal cancer cells, and promote cell apoptosis. The database prediction and dual-luciferase reporter gene assay showed that HMGB1 was the downstream target gene of miR-495-3p. We finally demonstrated that miR-495-3p inhibited CRC cell proliferation by targeting HMGB1 in vitro and in vivo.Conclusion: Our research shows that miR-495-3p inhibits the progression of colorectal cancer by down-regulating the expression of HMGB1, which indicates that miR-495-3p may become a potential therapeutic target for colorectal cancer.

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MiR-125b Inhibits Cell Proliferation and Induces Apoptosis in Human Colon Cancer SW480 Cells via Targeting STAT3

Recent Patents on Anti-Cancer Drug Discovery ◽

10.2174/1574892816666210708165037 ◽

2021 ◽

Vol 16 ◽

Author(s):

Junhe Zhang ◽

Wenwen Yang ◽

Yunxi Xiao ◽

Linlin Shan

Keyword(s):

Colon Cancer ◽

Cell Proliferation ◽

Cancer Cells ◽

Luciferase Reporter ◽

Colon Cancer Cells ◽

Luciferase Reporter Gene ◽

Luciferase Reporter Gene Assay ◽

Gene Assay ◽

Proliferation And Apoptosis ◽

Sw480 Cells

Background: Colon cancer is one of the most common types of cancer worldwide. Multiple studies have unveiled the key role of microRNAs (miRNAs) in the development of various types of cancer. However, the mechanism of action of miR-125b in the development and progression of colon cancer remains unknown. Objective: In this study, we explored the association of miR-125b and signal transducer and activator of transcription 3 (STAT3) and its role in the proliferation and apoptosis of SW480 colon cancer cells. Methods: The miR-125b expression in NCM460, SW480, HT29, and HCT8 cells was detected using quantitative real-time polymerase chain reaction (qRT-PCR). SW480 cells were transfected with lentiviruses of GFP–miR–125b and GFP–NC to establish a stable miR-125b overexpression colon cancer cell model and a control model. The targeting relationship between miR-125b and STAT3 was analyzed using bioinformatics and verified by the dual-luciferase reporter gene assay. Cell proliferation and apoptosis were assessed using the Cell Counting Kit-8 assay and TUNEL staining. The expression levels of STAT3, Bcl-2, and Bax were analyzed using Western blot analysis. Results: It was found that the relative mRNA expression of miR-125b was decreased in SW480, HT29, and HCT8 cells compared with that in NCM460 cells (P<0.05). The luciferase reporter gene assay confirmed that miR-125b downregulated the STAT3 gene expression (P<0.05). Overexpression of miR-125b inhibited proliferation and promoted apoptosis in SW480 colon cancer cells and was accompanied by upregulated Bax expression and downregulated Bcl-2 expression (P<0.05). Re-expression of STAT3 promoted cell proliferation and inhibited cell apoptosis, whereas Bcl-2 expression increased, and Bax expression decreased (P<0.05). Conclusion: The miR-125b regulates the expression of Bax and Bcl-2 by downregulating the expression of STAT3, thereby inhibiting proliferation and inducing apoptosis of SW480 colon cancer cells.

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Expression and role of miR-637 before and after lymphadenectomy for thyroid carcinoma

Materials Express ◽

10.1166/mex.2021.2053 ◽

2021 ◽

Vol 11 (7) ◽

pp. 1245-1253

Author(s):

Yanqing Qu ◽

Xiaoyu Chu ◽

Cuihong Dong ◽

Weijiao Wang ◽

Xiaojian Zhang

Keyword(s):

Cell Proliferation ◽

Thyroid Carcinoma ◽

Biological Significance ◽

Negative Control ◽

Luciferase Reporter ◽

Proliferation And Apoptosis ◽

Before And After ◽

Proliferation And Invasion

Thyroid carcinoma (TC) is a common endocrine malignancy that can be partially relieved by surgery, but its recurrence rate remains high. It is speculated that miR-637 exerts certain influence in its occurrence and development. Accordingly, we included 87 TC patients and 72 concurrent healthy controls as the research participants and purchased human papillary thyroid carcinoma cells with which to study and analyze the biological significance of miR-637. The determination of miR-637 and SH2B1 in peripheral blood and tissues was performed using nanoparticle-assisted polymerase chain reaction assay, and the identification of cell proliferation and apoptosis was made by MTT, Transwell, and flow cytometry. The results indicated that after transfection of miR-637 into TPC-1, the cell proliferation and invasion capacities in the mimics-miR-637 group were significantly reduced as compared to that of the inhibition-miR-637 and negative control (NC)-miR groups (P < 0.05). While transfection of SH2B1 into TPC-1 cells led to significantly enhanced cell proliferation and invasion capacities in sh-SH2B1 group than in si-SH2B1 and NC groups (P < 0.05). Finally, a double luciferase reporter assay identified enormously inhibited fluorescence activity of SH2B1-WT by mimics-miR-637. According to the experimental results, it is concluded that miR-637 expression was low in TC but increased after lymphadenectomy for TC. Moreover, by targeting SH2B1, miR-637 interferes with TC progression, which carries significant implications for future diagnosis and treatment of the disease.

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Glucocorticoid inhibits cell proliferation in differentiating osteoblasts by microRNA-199a targeting of WNT signaling

Journal of Molecular Endocrinology ◽

10.1530/jme-14-0314 ◽

2015 ◽

Vol 54 (3) ◽

pp. 325-337 ◽

Cited By ~ 30

Author(s):

Changgui Shi ◽

Ping Huang ◽

Hui Kang ◽

Bo Hu ◽

Jin Qi ◽

...

Keyword(s):

Cell Proliferation ◽

Wnt Signaling ◽

Transcriptional Repression ◽

Wnt Signaling Pathway ◽

Luciferase Reporter ◽

Osteoblast Proliferation ◽

Cellular Processes ◽

Proliferation And Apoptosis ◽

Proliferation Assays

The inhibition of osteoblast proliferation by glucocorticoids (GCs) is very important in the etiology of GC-induced osteoporosis. The mechanisms of this process are still not fully understood. The results of recent studies have indicated an important role for microRNAs in GC-mediated responses in various cellular processes, including cell proliferation and apoptosis. Therefore, we developed the hypothesis that these regulatory molecules might be involved in GC-decreased osteoblast proliferation. Western blotting, quantitative real-time PCR, cell proliferation assays, and luciferase assays were employed to investigate the role of miRNAs in GC-inhibited osteoblast proliferation. microRNA-199a-5p was significantly increased in osteoblasts treated with dexamethasone (Dex). To delineate the role of microRNA-199a-5p, we silenced and overexpressed microRNA-199a-5p in osteoblasts. We found that overexpressing microRNA-199a-5p remarkably increased the inhibition effect of Dex on osteoblast proliferation, and depleting microRNA-199a-5p significantly attenuated Dex-inhibited osteoblast proliferation. Results of mechanistic studies indicated that microRNA-199a-5p inhibited FZD4 and WNT2 expression through a microRNA-199a-5p binding site within the 3′-UTR of FZD4 and WNT2. The post-transcriptional repression of FZD4 and WNT2 were further confirmed by luciferase reporter assay. These results indicated that microRNA-199a-5p may play a significant role in GC-inhibited osteoblast proliferation by regulating the WNT signaling pathway.

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Differential Expression of miR-381-3p in Alzheimer’s Disease Patients and Its Role in Beta-Amyloid-Induced Neurotoxicity and Inflammation

NeuroImmunoModulation ◽

10.1159/000519780 ◽

2021 ◽

pp. 1-9

Author(s):

Meng Zhang ◽

Yonglei Liu ◽

Pingping Teng ◽

Qing Yang

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Cell Proliferation ◽

Inflammatory Cytokines ◽

Roc Curve ◽

Pearson Correlation ◽

Luciferase Reporter ◽

Cell Models ◽

Gene Assay ◽

Proliferation And Apoptosis

Introduction: This study aimed to explore the diagnostic value and effect of miR-381-3p on Alzheimer’s disease (AD). Methods: RT-qPCR was used for the measurement of miR-381-3p levels. Pearson correlation coefficient was used for the correlation analysis. Receiver operating characteristic (ROC) curve was constructed to assess the distinct ability of miR-381-3p for AD. SH-SY5Y cells were treated with Aβ25-35 to establish an AD cell model. The role of miR-381-3p on cell proliferation and apoptosis was detected. ELISA was applied to detect the protein levels of inﬂammatory cytokine expression. The target relationship of miR-381-3p with PTGS2 was verified by luciferase reporter gene assay. Results: Low expression of miR-381-3p was detected in the serum of AD patients and cell models. There was a negative association of serum miR-381-3p with the serum inflammatory cytokines. The ROC curve demonstrated the distinct ability of serum miR-381-3p for AD, with the AUC value of 0.898, with a sensitivity of 87.5%, and a specificity of 77.7%. Overexpression of miR-381-3p reversed the influence of Aβ25-35 on cell proliferation and apoptosis, but miR-381-3p downregulation exacerbated the influence. miR-381-3p overexpression inhibited the release of IL-6, IL-1β, and TNF-α induced by Aβ25-35 treatment, whereas miR-381-3p downregulation further promoted the release of inflammatory cytokines. PTGS2 was the target gene of miR-381-3p and was upregulated in AD cell models. Conclusion: miR-381-3p is less expressed in the serum of AD patients and has potential diagnostic values for AD. Overexpression of miR-381-3p may attenuate Aβ25-35-induced neurotoxicity and inflammatory responses via targeting PTGS2 in SH-SY5Y cells.

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CircRNA-MSR Regulates LPS-Induced C28/I2 Chondrocyte Injury through miR-643/MAP2K6 Signaling Pathway

Cartilage ◽

10.1177/19476035211044826 ◽

2021 ◽

pp. 194760352110448

Author(s):

Zhen Jia ◽

Qing-Jun Wei

Keyword(s):

Cell Proliferation ◽

Degenerative Joint Disease ◽

Mitogen Activated Protein Kinase ◽

Joint Disease ◽

Luciferase Reporter ◽

Circular Rnas ◽

Enzyme Linked Immunosorbent Assay ◽

Luciferase Reporter Gene ◽

Rna Fish

Objective Osteoarthritis (OA) is a degenerative joint disease characterized by deterioration of articular cartilage functions. Previous studies have confirmed the role of circular RNAs (circRNAs) in OA, but the role of mechanical stress–related circRNA (circRNA-MSR) in OA is unknown. Design The human chondrocytes C28/I2 were cultured and treated with lipopolysaccharide (LPS) to establish the OA model. The mRNA and protein levels were measured by qRT-PCR or Western blot. Cell viability was analyzed by MTT assay. Flow cytometry was carried out to detect cell apoptosis. The levels of TNF-α, IL-1β, and IL-6 were determined by enzyme-linked immunosorbent assay (ELISA). Pull-down assay was conducted to measure circRNA-MSR-related miRNA. Dual-luciferase reporter gene detection was performed to detect the target relationships between miR-643 and circRNA-MSR or Mitogen-activated protein kinase kinase 6 (MAP2K6). The RNA–fluorescence in situ hybridization (RNA-FISH) assay was conducted to verify the localization of circRNA-MSR and miR-643. Results The expressions of circRNA-MSR were upregulated in LPS stimulated C28/I2 cells. Knockdown of circRNA-MSR can inhibit LPS-induced apoptosis, inflammatory response, and extracellular matrix (ECM) degradation, and promote cell C28/I2 cells proliferation. Moreover, circRNA-MSR directly targeted miR-643. RNA-FISH exhibited that circRNA-MSR may act as a competing endogenous RNA (ceRNA) of miR-643. Over-expression of miR-643 could alleviate LPS-induced C28/I2 chondrocyte injury and promote cell proliferation. Besides, miR-643 directly bound to MAP2K6 mRNA. MiR-643 inhibition or MAP2K6 overexpression can reverse the role of circRNA-MSR knockdown on LPS-treated chondrocytes. Conclusion circRNA-MSR can upregulate MAP2K6 by targeting miR-643, thereby inhibiting cell proliferation and promoting apoptosis of C28/I2 cells.

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Effect of microRNA-21 on Proliferation and Apoptosis of Osteosarcoma Cells via Phosphatase and Tensin Homologue (PTEN)-Phosphoinositide 3-Kinase (PI3K)/AKT Pathway

Journal of Biomaterials and Tissue Engineering ◽

10.1166/jbt.2020.2293 ◽

2020 ◽

Vol 10 (4) ◽

pp. 512-517

Author(s):

Lei Huang ◽

Yongheng Xie ◽

Zilong Yao ◽

Bin Yu

Keyword(s):

Cell Proliferation ◽

Cell Apoptosis ◽

Akt Signaling ◽

Luciferase Reporter ◽

Osteosarcoma Cells ◽

Luciferase Reporter Gene ◽

Gene Assay ◽

Proliferation And Apoptosis ◽

Phosphoinositide 3 Kinase ◽

Phosphatase And Tensin Homologue

Objective: PTEN can inhibit the activity of PI3K/AKT signaling and regulate cell proliferation and apoptosis. Increased expression of microRNA-21 is associated with osteosarcoma. Bioinformatics analysis showed a targeted binding site between microRNA-21 and PTEN 3 -UTR. Our study assessed whether microRNA-21 regulates PTEN-PI3K/AKT signaling and affects the proliferation, cloning and apoptosis of osteosarcoma cells. Methods: Dual luciferase reporter gene assay was used to assess the targeted interaction between microRNA-21 and PTEN. Expression of microRNA21 and PTEN was measured in human normal osteoblasts hFOB1.19, osteosarcoma Saos-2 and MG-63. Saos-2 cells were cultured and divided into microRNA-NC group and microRNA-21 inhibitor group followed by measuring the expression of microRNA-21, PTEN and p-AKT, cell apoptosis by flow cytometry, cell proliferation by EdU staining and cloning ability by plate cloning. Results: There was a targeted relationship between microRNA-21 and PTEN. Compared with hFOB1.19 cells, microRNA-21 level in Saos-2 and MG-63 cells was increased and PTEN was decreased. Transfection of microRNA-21 inhibitor significantly reduced microRNA-21 level in Saos-2 cells, increased PTEN, decreased p-AKT, cell proliferation and cloning ability, as well as promoted cell apoptosis. Conclusion: The increased microRNA-21 expression may play a role in reducing PTEN level and promoting osteosarcoma pathogenesis. Inhibiting microRNA-21 can inhibit the activity of PTENPI3K/AKT signaling, reduce the proliferation and cloning ability of osteosarcoma cells, and promote cell apoptosis.

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Long noncoding RNA LINC00342 promotes growth of infantile hemangioma by sponging miR-3619-5p from HDGF

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00188.2019 ◽

2019 ◽

Vol 317 (4) ◽

pp. H830-H839 ◽

Cited By ~ 8

Author(s):

Zhen Liu ◽

Zhenming Kang ◽

Yujian Dai ◽

Huiming Zheng ◽

Yingjun Wang

Keyword(s):

Cell Proliferation ◽

Endothelial Cells ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Molecular Mechanisms ◽

Rna Binding ◽

Micro Rna ◽

Luciferase Reporter ◽

Proliferation And Apoptosis

Infantile hemangiomas (IH) are a type of benign vascular neoplasm that may cause permanent scarring. Hemangioma-derived endothelial cells (HemECs) are commonly used as an in vitro model to study IH. Long noncoding RNA is a type of RNA transcript longer than 200 nucleotides that does not encode any protein. LINC00342 was discovered to regulate proliferation and apoptosis in nonsmall cell lung cancer. However, the role of LINC00342 in IH has never been reported before. Expressions of LINC00342 and miR-3619-5p were detected in proliferating versus normal skin tissues. Colony formation and Cell-Couting Kit 8 assays were carried out to study the effects on cell proliferation after knockdown and overexpression of LINC00342, respectively. Meanwhile caspase-3 activity and nucleosomal fragmentation assay were applied to detect cell apoptosis. Micro-RNA binding sites on LINC00342 and hepatoma-derived growth factor (HDGF) were predicted and confirmed via dual-luciferase reporter assay. Biotin RNA pulldown assay was used to verify the direct binding between RNA molecules. LINC00342 enhanced proliferation and inhibited apoptosis in HemECs. MiR-3619-5p targeted both LINC00342 and HDGF, where LINC00342 sponged miR-3619-5p and positively regulated HDGF. HDGF knockdown rescued the effects of LINC00342 on HemECs. The LINC00342-miR-3619-5p-HDGF signaling pathway could regulate cell proliferation and apoptosis in HemECs. NEW & NOTEWORTHY The role of LINC00342 in infantile hemangiomas has not yet been elucidated. This paper highlights the regulatory role of LINC00342 in cell proliferation and apoptosis in hemangioma-derived endothelial cells and the underlying molecular mechanisms. The findings would provide potential target for treatment of infantile hemangiomas.

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Knockdown of lncRNA HOTTIP Inhibits Retinoblastoma Progression by Modulating the miR-101-3p/STC1 Axis

Technology in Cancer Research & Treatment ◽

10.1177/1533033821997831 ◽

2021 ◽

Vol 20 ◽

pp. 153303382199783

Author(s):

XiangWen Yuan ◽

Zhaoyan Sun ◽

Congxian Cui

Keyword(s):

Cell Proliferation ◽

Western Blotting ◽

Underlying Mechanism ◽

Luciferase Reporter ◽

Luciferase Reporter Gene ◽

Qrt Pcr ◽

Gene Assay ◽

Proliferation And Apoptosis ◽

Y79 Cells

Objective: Retinoblastoma (RB) is a frequent eye cancer in children. Long non-coding RNA (LncRNA) HOXA transcript at the distal tip (HOTTIP) is aberrantly expressed in cancer tissues. This study explores the underlying mechanism of lncRNA HOTTIP in RB. Methods: HOTTIP expression in normal retinal cells and RB cell lines was detected using qRT-PCR. The proliferation of RB cells was measured using CCK-8 and EdU assays, and apoptosis was detected using flow cytometry and Western blotting after the transfection of si-HOTTIP into Y79 cells and pc-HOTTIP into HXO-RB-44 cells. The target relationships between HOTTIP and miR-101-3p, and miR-101-3p and STC1 were predicted by bioinformatics website and verified using dual-luciferase reporter gene assay. The binding of HOTTIP and miR-101-3p was verified using RNA pull-down assay. STC1 mRNA and protein in RB cells were measured using qRT-PCR and Western blotting. Moreover, si-HOTTIP and in-miR-101-3p/in-NC, and si-HOTTIP and pc-STC1/pcDNA were co-transfected into Y79 cells respectively to evaluate cell proliferation and apoptosis. Xenograft study was conducted, and Ki67-positive expression was detected using immunohistochemical staining. Results: HOTTIP expression was promoted in RB tissues and cells. Downregulation of HOTTIP inhibited proliferation and promoted apoptosis of Y79 cells, while upregulation of HOTTIP promoted proliferation and inhibited apoptosis of HXO-RB-44 cells. There were target relationships between HOTTIP and miR-101-3p, and miR-101-3p and STC1. Inhibition of miR-101-3p or overexpression of STC1 reversed the effect of si-HOTTIP on the proliferation and apoptosis of RB cells. Xenograft study showed that knockdown of HOTTIP suppressed the growth of RB in vitro. Conclusion: It could be concluded that HOTTIP sponged miR-101-3p to upregulate STC1 expression, thereby promoting RB cell proliferation and inhibiting apoptosis.

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