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. 2019 Sep;44(3):973-981.
doi: 10.3892/ijmm.2019.4258. Epub 2019 Jun 27.

miR-92a-3p promotes the proliferation, migration and invasion of esophageal squamous cell cancer by regulating PTEN

Xin Li  1 , Shuilong Guo  2 , Li Min  2 , Qingdong Guo  2 , Shutian Zhang  2
Affiliations

miR-92a-3p promotes the proliferation, migration and invasion of esophageal squamous cell cancer by regulating PTEN

Xin Li et al. Int J Mol Med. 2019 Sep.

Retraction in

Abstract

Esophageal squamous cell cancer (ESCC) has a high mortality rate. MicroRNA (miR)‑92a‑3p is considered to be a tumor promotor and an oncomiR. The aim of the present study was to investigate the effect of miR‑92a‑3p and its target gene on ESCC in terms of proliferation, migration and invasion. Higher expression of miR‑92a‑3p was detected in the tissues of patients with ESCC, compared with that in normal tissues. In addition, ESCC cell lines had a higher expression of miR‑92a‑3p compared with normal esophageal cells. A miR‑92a‑3p mimic was found to promote ESCC cell proliferation and a miR‑92a‑3p inhibitor was found to reduce ESCC cell proliferation. miR‑92a‑3p mimic transfection accelerated ESCC cell migration and invasion and decreased ESCC cell apoptosis via the Bax/Bcl‑2 pathway and cleaved caspase‑3. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) was detected as a target of miR‑92a‑3p by a dual luciferase reporter assay. The overexpression of PTEN not only inhibited ESCC proliferation, migration and invasion, but also promoted ESCC cell apoptosis. PTEN and the miR‑92a‑3p mimic inhibited and promoted ESCC proliferation, respectively, which may be associated with the PI3K/Akt pathway. The results of the study revealed that miR‑92a‑3p promoted the proliferation, migration and invasion of ESCC, and the effect of miR‑92a‑3p on ESCC was realized by regulating PTEN.

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Figures

Figure 1
Figure 1
Effects of miR-92a-3p mimic and miR-92a-3p inhibitor on the proliferation of ESCC cells. (A) Expression levels of miR-92a-3p in tissues from patients with ESCC were measured by RT-qPCR. (B) Expression of miR-92a-3p in HET-1A cells (normal esophageal cells) and ESCC cells (Eca-109, EC9706, KYSE-30, KYSE-150, KYSE-220 and KYSE-510 cells) were determined using RT-qPCR. (C) Effects of miR-92a-3p mimic and miR-92a-3p inhibitor on the expression of miR-92a-3p in Eca-109 cells. A cell counting kit-8 was used to detect cell proliferation 24, 48 and 72 h after transfection with (D) miR-92a-3p mimic or (E) miR-92a-3p inhibitor into Eca-109 cells. The values are presented as the mean ± SD. Student's t-test was used to analyze differences between two groups. *P<0.05 and **P<0.01 vs. control group; #P<0.05 and ##P<0.01 vs. mimic control group; ^P<0.05 and ^^P<0.01 vs. inhibitor control group. miR, microRNA; ESCC, esophageal squamous cell cancer; RT-qPCR, reverse transcription-quantitative polymerase chain reaction.
Figure 2
Figure 2
Effects of miR-92a-3p mimic and miR-92a-3p inhibitor on Eca-109 apoptosis. miR-92a-3p mimic or miR-92a-3p inhibitor were transfected into Eca-109 cell for 48 h. (A) Cell apoptosis and (B) apoptotic rates were determined using an Annexin V FITC and PI assay. (C) Cell protein was extracted using lysis solution, and the levels of proteins (Bcl-2, Bax and cleaved caspase-3) were determined by western blotting following (D) mimic and (E) inhibitor treatment. The values are presented as the mean ± SD. Student's t-test was used to analyze the differences between two groups. *P<0.05 and **P<0.01 vs. Blank group; #P<0.05 and ##P<0.01 vs. mimic control group; ^^P<0.01 vs. inhibitor control group. miR, microRNA; PI, propidium iodide.
Figure 3
Figure 3
Effects of miR-92a-3p mimic and miR-92a-3p inhibitor on Eca-109 migration and invasion. miR-92a-3p mimic or miR-92a-3p inhibitor were trans-fected into Eca-109 cells for 48 h. (A) A scratch assay determined the Eca-109 cell migration ability and (B) rates were quantified. (C) Matrigel and Transwell assays were used for the determination of Eca-109 invasion ability. (D) Images showing staining for cell invasion. The values are presented as the mean ± SD. Student's t-test was used to analyze differences between two groups. **P<0.01 vs. Blank group; ##P<0.01 vs. mimic control group; ^^P<0.01 vs. inhibitor control group. miR, microRNA.
Figure 4
Figure 4
Overexpression of PTEN inhibits Eca-109 proliferation. (A) TargetScan 7.2 predicted the target gene of miR-92a-3p. (B) miR-92a-3p was overex-pressed in mimic group. (C) A dual luciferase reporter assay was used to determine the association between PTEN and miR-92a-3p. (D) PTEN, miR-92a-3p mimic and their combination were transfected into Eca-109 cells for 48 h, and the protein level of PTEN was analyzed by western blotting and quantitation. (E) Cell proliferation was detected using a cell counting kit-8. The values are presented as the mean ± SD. Student's t-test was used to analyze differences between two groups. **P<0.01 vs. blank group; aP<0.05 and aaP<0.01 vs. NC group; bP<0.05 and bbP<0.01 vs. PTEN group; ccP<0.01 vs. mimic + NC group. miR, microRNA; PTEN, phosphatase and tensin homolog deleted on chromosome 10; WT, wild-type; MUT, mutant; 3′UTR, 3′ untranslated region; Blank, untransfected cells; NC, cells transfected with empty vector; PTEN, cells transfected with PTEN recombinant plasmid; mimic + NC, cells transfected with mimics and empty vector; mimic + PTEN, cells transfected with mimic and PTEN recombinant plasmid.
Figure 5
Figure 5
Effects of the overexpression of PTEN on Eca-109 migration, invasion and apoptosis. PTEN, miR-92a-3p mimic and their combination were transfected into Eca-109 for 48 h. (A) A scratch assay determined Eca-109 cell migration ability. (B) Matrigel and Transwell assays were used to detect the cell invasion ability. (C) Cell apoptosis was determined using an Annexin V FITC/PI assay. The values are presented as the mean ± SD. Student's t-test was used to analyze differences between two groups. aP<0.05 and aaP<0.01 vs. NC group, bP<0.05 and bbP<0.01 vs. PTEN group; cP<0.05 and ccP<0.01 vs. mimic + NC group. miR, microRNA; PTEN, phosphatase and tensin homolog deleted on chromosome 10; NC, cells transfected with empty vector; PI, propidium iodide.
Figure 6
Figure 6
Overexpression of PTEN inhibits the PI3K/Akt pathway in Eca-109 cells. PTEN, miR-92a-3p mimic and their combination was transfected into Eca-109 cells for 48 h. (A) Protein levels of p-PI3K, PI3K, p-Akt and Akt were measured by western blotting and (B) quantification. (C) IGF-1, activator of the PI3K/Akt pathway, alone and in combination was used to treat Eca-109 cell for 48 h, and a cell counting kit-8 assay detected cell proliferation. The values are presented as the mean ± SD. Student's t-test was used to analyze differences between two groups. *P<0.05 vs. Blank group, aaP<0.01 vs. NC group, bP<0.05 and bbP<0.01 vs. PTEN group, ccP<0.01 vs. mimic + NC group; eP<0.05 vs. IGF-1 group; fP<0.05 vs. mimic + IGF-1 group. PTEN, phosphatase and tensin homolog deleted on chromosome 10; p-, phosphorylated; NC, cells transfected with empty vector; IGF-1, insulin-like growth factor 1.
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