Study on the mechanism behind lncRNA MEG3 affecting clear cell renal cell carcinoma by regulating miR‐7/RASL11B signaling

Abstract

The goal of this research was to study the relationships between maternally expressed gene 3 (MEG3), microRNA-7 (miR-7), and RASL11B, and explore their influence on the progression of clear cell renal cell carcinoma (CCRCC). Microarray analysis was conducted using the data provided by The Cancer Genome Atlas. The expression levels of MEG3 and miR-7 in CCRCC and adjacent tissue samples were ascertained by quantitative real-time polymerase chain reaction (qRT-PCR). The cell proliferation activity was unmasked by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, and cell apoptosis and cell cycle were investigated by flow cytometry. A dual luciferase reporter assay was used to verify target relationships. Wound healing assay and transwell assay were used to detect cell migration and invasion ability. Decreased MEG3 expression was observed in CCRCC tissues and cells. Overexpression of MEG3 accelerated apoptosis; inhibited cell proliferation, migration and invasion; and induced G0/G1 phase cell cycle arrest in CCRCC. MiR-7, directly binding to MEG3, was overexpressed in the CCRCC tissues and could inhibit the apoptosis and promote the migration and invasion of CCRCC cells. RASL11B, lowly expressed in CCRCC, was a target of miR-7. After the overexpression of RASL11B, G0/G1 phase cell cycle arrest was induced; cell apoptosis was promoted; and the proliferation, invasion, and migration of CCRCC cells were inhibited. MEG3 could up-regulate RASL11B to inhibit the cell proliferation, invasion, and migration; induce G0/G1 cell cycle arrest; and promote cell apoptosis by suppressing miR-7 in CCRCC.

Application of cAMP-dependent catalytic subunit β (PRKACB) Low Expression in Predicting Worse Overall Survival: A Potential Therapeutic Target for Colorectal Carcinoma

“…Gene co-expression network analysis established that PRKACB had a completely positive correlation with FAM167A, NRIP3, RASL11B, ST13P4, TMEM99, and a completely negative correlation with ALPP, C3ORF70, JUND, and ZBTB7A. It has been confirmed by studies that NRIP3 and RASL11B play a role in suppressing cancer proliferation in breast cancer and renal cell carcinoma [31,32]. Meanwhile ALPP, JUND, ZBTB7A in gastric cancer, prostate cancer, breast cancer [33][34][35] and other cancers promote the progress of cancer.…”

Revisiting Cell Death Responses in Fibrotic Lung Disease: Crosstalk between Structured and Non-Structured Cells

“…These findings are important because if the specific sets of antigens can reflect the ongoing pathophysiological processes that are upregulated in fibrotic lesions, we can determine the molecular events that occur in the disease environment through examination of patient sera [12]. Sera from IPF patients react with molecules associated with TGF-β and fibroblast activation (transgelin 2 [83], transgelin 3 [84], LIM domain-binding protein 2 [85], HLA complex P5 [86], PHGDH [87], NAT6 [88], CDK9 [89], SEPT4 [90]), cell death regulation (14-3-3 protein zeta/delta [91], Trefoil factor 2 protein [92], RAS-like family 11 member B [93], MRPS11 [94], RSU1 [95], PLCG2 [96], IFI44L [97], YTHDF2 [98], AMOTL2 [99], ROGDI [100]), and airway clearance (sperm flagellar 1 [101], cilia and flagella associated protein 410 [102], t-complex 10 like [103]) ( Table 1). Natural autoantibodies are thought to reflect the ongoing disease environment [10,11].…”

Natural Autoantibodies in Chronic Pulmonary Diseases

“…This finding is promising because if these sets of antigens reflect the molecules that constitute and are upregulated in IPF or INSIP lesions, we can determine which molecular events occur in IPF and INSIP lesions. IPF patient sera reacts with TGF-β-associated molecules (transgelin 2 (TAGLN2), transgelin 3 (TAGLN3) [23], LIM domain-binding protein 2 (LDB2) [24], and HLA complex P5 (HCP5) [25]), regulators of apoptotic pathways (14-3-3 protein zeta/delta (YWHAZ) [26], Trefoil factor 2 protein (TFF2) [27], and RAS-like family 11 member B (RASL11B) [28]), and proteins necessary for cilia formation and maintenance {sperm flagellar 1 (SPEF1) [29], cilia and flagella associated protein 410 (CFAP410)}, and other molecules important for cellular pathways that are also associated with disease development, such as regulating synaptic membrane exocytosis 4 (RIMS4) [30], mitochondrial ribosomal protein S11 (MRPS11) [31], and Ras suppressor-1 (RSU-1) [32]. In INSIP patients, aminoacyl tRNA synthases (glutaminyl-tRNA synthetase (QARS), glycyl-tRNA synthetase (GARS), and methionyl-tRNA synthetase (MARS) [18]), interferon-related molecules (MX1 [12], radical S-adenosyl methionine domain containing 2 (RSAD2) [33], and ninjurin 2 (NINJ2) [34]), and molecules associated with tissue repair (cyclin-dependent kinase 1 (CDK1) [35], retinoid X receptor alpha (RXRA) [36], CDC42 small effector protein 2 (CDC42SE) [37], and poly (ADP-ribose) glycohydrolase (PARG) [38]) are the targets of natural autoantibodies (Table 1).…”

“…IPF TAGLN2, TAGLN3 [23], LDB2 [24], HCP5 [25], YWHAZ [26], TFF2 [27], RASL11B [28], RIMS4 [30], MRPS11 [31], RSU1 [32], PLCG2, CCDC32, SPEF1 [29], CFAP410, ORMDL1, IFI44L, FTSJ1, POLR3K, POLR2L, TCP10L, PHGDH, YTHDF2, METTL21A, METTL14, STK31, NAT6, KCTD14, NIF3L1, CDK9, SEPT4, TIMMDC1, NECAB2, ZNF449, RECQL5, AMOTL2, ROGDI, SUPT4H1 TMEM254, PROK1 [39], CRCP [40] INSIP QARS, GARS, MARS [18], MX1 [12], RSAD2 [33], NINJ2 [34,41], CDK1 [35], RXRA [36], CDC42SE [37], PARG [38], PEX2, HK1, DCX, ABI1, BUD31, CCDC106, UCMA, ZMAT4, CTSC, TPRXL, NSL1, ALKBH3, ACO2, TCP11L1, NUBPL, ANXA6, TECR, KIF26A, MAPK10, PRKCZ, KCMF1, EIF5, DDI1, RIBC1, PARVA, CYB5R1, TPD52L3, EME1, TBC1D10C, RBFA, SHMT2, GPT2, STK39, MRPL1, PAPSS2…”