Influence of YKL‑40 gene RNA interference on the biological behaviors of endometrial cancer HEC‑1A cells

Abstract

The present study aimed to investigate the effects of chitinase-3-like protein 1 (YKL-40) gene RNA interference on the biological behaviors and enhanced chemosensitivity of endometrial cancer (EC) HEC-1A cells. YKL-40 small interfering (si)RNA was transduced into EC HEC-1A cells using a lentivirus. The experiment was divided into three groups: The experimental group was transfected with YKL-40 siRNA (si-YKL-40); the mock-treatment group was transfected with transfection reagent only; and the blank control group was left untreated. A reverse transcription-quantitative polymerase chain reaction was performed to investigate the mRNA expression levels of YKL-40. The biological behaviors, including cell proliferation, migration, invasion and apoptosis, were detected by MTT and Transwell assays, and flow cytometry (FCM) analysis, respectively. The results of the present study demonstrated that the mRNA expression levels of YKL-40 were downregulated within HEC-1A cells upon transfection with si-YKL-40 (P<0.05). The proliferative, migratory and invasive abilities of HEC-1A cells were inhibited by si-YKL-40 (P<0.05). The mRNA expression levels of YKL-40 were upregulated within HEC-1A cells following treatment with cisplatin (P<0.05). FCM analysis revealed that the average cellular apoptosis rate increased following the inhibition of YKL-40 gene expression via siRNA (P<0.05). Therefore, the YKL-40 gene may be associated with the proliferative, migratory, invasive and anti-apoptotic ability of HEC-1A cells. YKL-40 downregulation may enhance the sensitivity of human EC HEC-1A cells to chemotherapy.

Exosomal lncRNA NEAT1 from cancer-associated fibroblasts facilitates endometrial cancer progression via miR-26a/b-5p-mediated STAT3/YKL-40 signaling pathway

“…So far, the detailed mechanisms of NEAT1 in EC have not been clarified. Previous studies have reported that YKL-40 contributed to the progression of EC and might be a prognostic indicator for EC [ 8 , 28 , 29 ]. In the present study, the results revealed that exosomal NEAT1 promoted YKL-40 expression in recipient HEC-1A and RL95-2 cells, however GW4869 or si-Rab27a-mediated suppression of exosome release reversed this result.…”

“…Li et al. indicated that depletion of YKL-40 led to a remarkable inhibition of growth and invasion in EC HEC-1A cells [8] . These findings strongly revealed that YKL-40 was essential for the malignant development of EC.…”

Knockdown of YKL‐40 inhibits angiogenesis through regulation of VEGF/VEGFR2 and ERK1/2 signaling in endometrial cancer

“…Recent studies have proposed that YKL‐40 plays a prominent role in cell proliferation, differentiation, angiogenesis, tissue remodeling, inflammation, and antiapoptosis (Johansen et al, 2007; Johansen et al, 2009; Kazakova & Sarafian, 2009). Other studies also found that YKL‐40 was associated with the prognosis of EC patients, and the increased levels of YKL‐40 in EC predicted poor clinical outcomes, which also influenced the proliferative, migratory, invasive, and antiapoptotic ability of HEC‐1A cells (Kotowicz et al, 2017; Lili Li et al, 2018). However, the molecular mechanisms for YKL‐40 in EC are not yet clear.…”

“…It was observed that small interfering RNA (siRNA) targeting YKL‐40 (si YKL‐40 ) could inhibit the proliferation, migration, and invasion of HEC‐1A cells (Li et al, 2016). It was also found that YKL‐40 was upregulated in EC and was correlated with the poor prognosis (Li et al, 2018). Besides, the inhibition of YKL‐40 could suppress the cell proliferation, migration, and invasion of EC cells and would reduce the sensitivity to cisplatin (Li et al, 2018).…”

“…It was also found that YKL‐40 was upregulated in EC and was correlated with the poor prognosis (Li et al, 2018). Besides, the inhibition of YKL‐40 could suppress the cell proliferation, migration, and invasion of EC cells and would reduce the sensitivity to cisplatin (Li et al, 2018). However, the molecular mechanisms of YKL‐40 in EC, such as in angiogenesis, remain uncertain and need to be further explored.…”