Latest Breaking News On - Chinese academy of sciences shanghai - Page 5 : comparemela.com
1
2Medical Records Management Division, Chongqing University Cancer Hospital, Chongqing, People’s Republic of China;
3Intensive Care Unit, Chongqing University Cancer Hospital, Chongqing, People’s Republic of China;
4Pharmacy Services, Chongqing University Cancer Hospital, Chongqing, People’s Republic of China These authors contributed equally to this work
Correspondence: Dehong Huang
Department of Hematology and Oncology, Chongqing University Cancer Hospital, No. 181 Hanyu Road, Chongqing, People’s Republic of China
Tel +86 23-65311341
Purpose: This study investigated the function and molecular mechanisms of miR-744-5p in multiple myeloma (MM).
Methods: miR-744-5p and SRY-related high-mobility-group box 12 (SOX12) expression in clinical tissues and MM cells was monitored by quantitative real-time polymerase chain reactions and Western blot. miR-744-5p expression in MM cells was regulated by transfection. Cell proliferation was researched by cell counting kit-8 as
WalthamLeicestershireUnited-kingdomShigaJapanTokyoUnited-statesShanghaiChinaBeijingWisconsinHelsinkiReverse Transcription Quantitative PCR (RT-qPCR)
Following total RNA extraction using TRIzol reagent (Invitrogen), cDNA was synthesized using Mir-X miRNA First-Strand Synthesis Kit (Takara Holdings Inc., Kyoto, Japan) with extracted total RNA (2 μg). The miRNA expression was measured by qPCR with SYBR Advantage qPCR Premix (Takara) on CFX133a Real-Time PCR Detection System (Bio-Rad Laboratories, Hercules, CA, USA). Relative expression was determined with a U6 control through the 2
−ΔΔCt method. The primers used are depicted in Table 1.
Table 1 Primer Sequences
Cell Culture, Transfection and Infection
Human lung cancer cell lines, including H522, H460, SK-MES-1, and A549, and a human bronchial epithelial cell line BEAS-2B, were from the Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences (Shanghai, China). Cell lines H522, H460, and A549 were cultivated in RPMI-1640 medium (Gibco; Thermo Fisher Scientific), while SK-MES-1 cells were in minimal medium (Gib
ZhengzhouHenanChinaUnited-statesChangshaHunanJapanTokyoShanghaiBeijingRotkreuzSwitzerland-generalG) The mRNA and (
H,
I) protein levels of CCND1 were determined by Real-Time qPCR and Western Blot analysis, respectively. (Note: “Con” indicated “Control”, “KD-L” indicated “Knock-down of LncRNA SNHG16” and “KD-L+KD-miR” suggested “both LncRNA SNHG16 and miR-17-5p ablation”). Each experiment repeated at least 3 times, and
P 0.05.
Knock-Down of LncRNA SNHG16 Inhibited OSCC Progression Through the miR-17-5p/CCND1 Axis
We next investigated whether LncRNA SNHG16 regulated OSCC development by targeting the miR-17-5p/CCND1 axis. To achieve this, the LncRNA SNHG16 silencing vectors, miR-17-5p inhibitor and CCND1 overexpression vectors were delivered into OSCC cells (Figure 6A and B), which were divided into four groups, including Control, KD-SNHG16, KD-SNHG16+miR-17-5p inhibitor, and KD-SNHG16+OE-CCND1. As expected, the data in Figure 6C and D showed that knock-down of LncRNA SNHG16 inhibited cell proliferation in OSCC cells, which were restored by silenci
XiangyaGuangdongChinaHelsinkiEteläuomen-läiFinlandShanghaiUnited-statesChineseAmericanCorning-co