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Study things to guide evidence-informed policies along with support with regard to usage of secure abortion treatment within sub-Saharan The african continent.
could further accelerate tumor proliferation, migration and invasion. It may serve as a therapeutic marker for liver cancer treatment.
For the first time, we found that RIZ1 was upregulated in liver cancer cells and RIZ1-mediated H3K9me1 enrichment on the HOTAIRM1 promoter regulated the growth and metastasis of liver cancer cells by targeting miR-125b, which could further accelerate tumor proliferation, migration and invasion. see more It may serve as a therapeutic marker for liver cancer treatment.
Amongst noncoding RNAs, competing endogenous RNAs (ceRNAs) are popular and interesting regulatory mechanisms involved in oncogenesis and tumour progression. LncRNA FGD5-AS1, also known as miR-5590-3p, is involved in the regulatory role of ceRNA in many cancers. However, the roles of lncRNA FGD5-AS1 or miR-5590-3p in renal cell carcinoma (RCC) remain unclear. We investigated how FGD5-AS1 and miR-5590-3p regulated clear cell proliferation and metastasis in RCC.

Real Time-quantitative PCR (RT-qPCR) was used to detect the expression of FGD5-AS1 in tumour issues and renal cancer cell lines. MTT, scratch test and transwell assay were performed to confirm the effect of FGD5-AS1 on the proliferation, migration or invasion of the above cell lines. RNA pull-down and Luciferase assays were used to detect the target site between FGD5-AS1 and miR-5590-3p. In addition, we examined the proteins related to ERK/AKT signalling related via Western blot analysis. Finally, we used the RT-qPCR method to detect the mRNA levels malignancy of tumours. This lncRNA could become a potential target molecule for treating and diagnosing RCC.
It was the aim of this study to explore the role and mechanism of long non-coding RNA (lncRNA) AFAP1-AS1 in the progression of bladder cancer (BCa) by in vitro experiments.

AFAP1-AS1 levels in 40 pairs of clinical BCa tissue samples and normal ones collected from BCa patients were determined, and paired sample t-test was applied to compare the differences between groups. The prognosis data of patients with BCa were collected, and survival analysis and t-test were performed to specify the interplay between AFAP1-AS1 and the prognosis of BCa patients. Subsequently, AFAP1-AS1 expression level in BCa and normal cells were further confirmed by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR), and Cell Counting Kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU), and transwell assays were performed to figure out the influence of this lncRNA on the proliferation ability and invasiveness of BCa cells. Meanwhile, the interaction between AFAP1-AS1 and its sense mRNA was analyzed. We used co-transfection technotion of AFAP1-AS1. Meanwhile, a negative interplay was discovered between AFAP1-AS1 and its sense mRNA. Finally, the results of cell reversal experiment using co-transfection technique revealed that overexpression of AFAP1 can reverse the inhibitory impact of lncRNAAFAP1-AS1 on the malignant ability of BCa cells.

AFAP1-AS1 may enhance the proliferation ability as well as the invasiveness of BCa cells so as to aggravate the degree of BCa malignancy.
AFAP1-AS1 may enhance the proliferation ability as well as the invasiveness of BCa cells so as to aggravate the degree of BCa malignancy.
This study aims to uncover the in vitro influences of lncRNA TMPO-AS1 on the progression of bladder cancer (BLCA) and the underlying mechanism.

Expression levels of TMPO-AS1 in BLCA tissues and normal bladder tissues were analyzed in The Cancer Genome Atlas (TCGA) database. Differential expressions of TMPO-AS1 in BLCA tissues and normal bladder epithelial tissues were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Potential influence of TMPO-AS1 on prognosis of BLCA patients was assessed. In vitro influences of TMPO-AS1 on proliferative and migratory abilities in T24 and UMUC-3 cells were evaluated by Cell Counting Kit-8 (CCK-8), transwell, and wound healing assay, respectively. Finally, the correlation between TMPO-AS1 and its sense RNA TMPO was assessed by analyzing TCGA database, clinical samples, and BLCA cell lines.

By analyzing TCGA database and clinical samples, it was found that TMPO-AS1 was upregulated in BLCA tissues compared with that in normal bladder tissues. Worse survival was observed in BLCA patients with high expression of TMPO-AS1. TMPO-AS1 level was correlated to muscle invasiveness and TNM stage of BLCA patients. In T24 and UMUC-3 cells, the knockdown of TMPO-AS1 suppressed proliferative and migratory abilities. TMPO-AS1 level was positively correlated to that of its sense RNA TMPO. Moreover, the knockdown of TMPO-AS1 downregulated mRNA and protein levels of TMPO in BLCA cells.

TMPO-AS1 is upregulated in BLCA tissue and closely linked to poor prognosis of BLCA patients.
TMPO-AS1 is upregulated in BLCA tissue and closely linked to poor prognosis of BLCA patients.
This study aims to explore the role of microRNA-320c (miR-320c) in regulating biological behaviors of cervical cancer and the potential mechanism, thus providing experimental references for developing therapeutic target of cervical cancer.

Differential expressions of miR-320c in cervical cancer samples and normal cervical tissues were determined. Potential association between miR-320c level and clinical characteristics of cervical cancer patients was analyzed. After overexpression of miR-320c, migratory potential changes in HeLa, and C33-A cells were examined. At last, target gene binding to miR-320c was predicted online and its involvement in the malignant development of cervical cancer was finally explored.

It was found that miR-320c was lowly expressed in cervical cancer tissues. Compared with cervical cancer patients with high expression of miR-320c, those with low expression had higher rates of lymphatic metastasis and distant metastasis. Besides, the overexpression of miR-320c markedly inhibited migratory potential in HeLa and C33-A cells. GABRP was verified to be the target gene binding to miR-320c. Notably, GABRP was able to reverse the role of miR-320c in regulating migratory potential in cervical cancer.

MiR-320c is capable of inhibiting migratory potential in cervical cancer by targeting GABRP, which may be utilized as a therapeutic target of cervical cancer.
MiR-320c is capable of inhibiting migratory potential in cervical cancer by targeting GABRP, which may be utilized as a therapeutic target of cervical cancer.
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