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Long non‑coding RNA KCNQ1OT1 promotes ovarian cancer cell malignant characteristics by targeting the miR‑140‑5p/KLK10 axis

  • Authors:
    • Renjie Duan
    • Zhenyu Tao
    • Shun Tao
    • Aichen Yang
    • Xu Yang
    • Changzheng Li
    • Xiaoxiang Zhu
    • Kexin Zhang
    • Zhuofu Li
    • Shanjun Tao
  • View Affiliations / Copyright

    Affiliations: School of Preclinical Medicine, Wannan Medical College, Wuhu, Anhui 241002, P.R. China, School of Pharmacy, Wannan Medical College, Wuhu, Anhui 241002, P.R. China, School of Laboratory Medicine, Wannan Medical College, Wuhu, Anhui 241002, P.R. China, School of Clinical Medicine, Wannan Medical College, Wuhu, Anhui 241002, P.R. China
    Copyright: © Duan et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 4.0].
  • Article Number: 134
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    Published online on: March 11, 2026
       https://doi.org/10.3892/etm.2026.13129
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Abstract

Long non‑coding RNAs (lncRNAs) have emerged as key regulatory molecules involved in driving cancer progression. However, the specific functional roles of numerous lncRNAs in ovarian cancer (OC) remain largely underexplored. The present study aimed to elucidate the role and underlying mechanisms of potassium voltage‑gated channel subfamily Q member 1 opposite strand/antisense transcript 1 (KCNQ1OT1) in OC progression. Bioinformatics prediction using the TargetScan and starBase databases revealed that both KCNQ1OT1 and kallikrein‑related peptidase 10 (KLK10) harbor complementary binding sites for microRNA (miR)‑140‑5p. The direct interaction between miR‑140‑5p and KCNQ1OT1 or KLK10 was experimentally validated using miRNA pull‑down assays. Analysis of GEO datasets (GSE66957 and GSE47841), followed by RT‑qPCR validation in SKOV3 and IOSE80 cells, revealed that KCNQ1OT1 and KLK10 were markedly upregulated, whereas miR‑140‑5p was downregulated in OC compared with that in normal ovarian controls. CCK‑8 and wound‑healing assays demonstrated that silencing KCNQ1OT1 markedly suppressed OC cell proliferation and migration, effects that were reversed by miR‑140‑5p inhibition. Conversely, inhibition of miR‑140‑5p enhanced OC cell proliferation and migration, which were abrogated by KLK10 knockdown. Collectively, these findings identified a previously unrecognized regulatory axis in OC, in which KCNQ1OT1 promotes tumor cell proliferation and migration by modulating the miR‑140‑5p/KLK10 pathway. The present study advances the mechanistic understanding of lncRNA‑mediated oncogenesis and provides preliminary evidence supporting a potential role of KCNQ1OT1 in OC progression.
View Figures

Figure 1

Expression of target genes in OC
datasets and cell lines. Principal component analysis plots showing
expression patterns in the (A) GSE66957 and (C) GSE47841 datasets.
Volcano plots illustrating differentially expressed genes in the
(B) GSE66957 and (D) GSE47841 datasets. Differential expression of
(E) KCNQ1OT1 (GSE66957), (F) KLK10 (GSE66957) and (G) miR-140-5p
(GSE47841). (H) Relative expression levels of KCNQ1OT1, KLK10 and
miR-140-5p in SKOV3 OC cells and IOSE80 normal ovarian epithelial
cells. *P<0.05 and **P<0.01. OC,
ovarian cancer; KCNQ1OT1, potassium voltage-gated channel subfamily
Q member 1 opposite strand/antisense transcript 1; KLK10,
kallikrein-related peptidase 10; miR, microRNA; Dim, dimension; FC,
fold change.

Figure 2

Validation of the binding
interactions between miR-140-5p, KCNQ1OT1 and KLK10. Predicted
binding sites of (A) KCNQ1OT1 with miR-140-5p and (B) miR-140-5p
with KLK10. (C) Enrichment of KCNQ1OT1 and KLK10 in pull-down
assays with Bio-miR-140-5p or Bio-NC. **P<0.01.
KCNQ1OT1, potassium voltage-gated channel subfamily Q member 1
opposite strand/antisense transcript 1; KLK10, kallikrein-related
peptidase 10; miRNA/miR, microRNA; NC, negative control; Bio,
biotin.

Figure 3

Roles of miR-140-5p and KLK10 in OC
cell proliferation and migration. Transfection with miR-140-5p
mimic suppressed KLK10 expression at both (A) mRNA and (B) protein
levels in OC cells. (C) Both miR-140-5p mimic and si-KLK10 reduced
cell proliferation. (D) Knockdown of KLK10 counteracted the
proliferative effect induced by miR-140-5p inhibitor. (E)
Wound-healing assay and (F) quantification showing that miR-140-5p
mimic or si-KLK10 inhibited cell migration, while KLK10 silencing
reversed the promigratory effect of miR-140-5p inhibitor. Scale
bar, 200 µm. *P<0.05 and **P<0.01. miR,
microRNA; OC, ovarian cancer; si, small interfering; KLK10,
kallikrein-related peptidase 10; NC, negative control; in,
inhibitor; OD, optical density.

Figure 4

KCNQ1OT1 knockdown inhibits OC cell
proliferation and migration by upregulating miR-140-5p. (A)
Transfection with si-KCNQ1OT1 elevated miR-140-5p expression levels
while reducing KLK10 mRNA levels in OC cells. (B) si-KCNQ1OT1
decreased KLK10 protein expression and this effect was
significantly reversed by co-transfection with miR-140-5p
inhibitor. (C) si-KCNQ1OT1 suppressed cell proliferation, whereas
co-transfection with miR-140-5p inhibitor ameliorated this effect.
(D) Wound-healing assay and (E) quantification showing that
si-KCNQ1OT1 inhibited cell migration with co-transfection with
miR-140-5p inhibitor counteracting this effect. Scale bar, 200 µm.
**P<0.01. miR, microRNA; OC, ovarian cancer; si,
small interfering; KCNQ1OT1, potassium voltage-gated channel
subfamily Q member 1 opposite strand/antisense transcript 1; KLK10,
kallikrein-related peptidase 10; NC, negative control; in,
inhibitor; OD, optical density.
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Copy and paste a formatted citation
Spandidos Publications style
Duan R, Tao Z, Tao S, Yang A, Yang X, Li C, Zhu X, Zhang K, Li Z, Tao S, Tao S, et al: Long non‑coding RNA KCNQ1OT1 promotes ovarian cancer cell malignant characteristics by targeting the miR‑140‑5p/KLK10 axis. Exp Ther Med 31: 134, 2026.
APA
Duan, R., Tao, Z., Tao, S., Yang, A., Yang, X., Li, C. ... Tao, S. (2026). Long non‑coding RNA KCNQ1OT1 promotes ovarian cancer cell malignant characteristics by targeting the miR‑140‑5p/KLK10 axis. Experimental and Therapeutic Medicine, 31, 134. https://doi.org/10.3892/etm.2026.13129
MLA
Duan, R., Tao, Z., Tao, S., Yang, A., Yang, X., Li, C., Zhu, X., Zhang, K., Li, Z., Tao, S."Long non‑coding RNA KCNQ1OT1 promotes ovarian cancer cell malignant characteristics by targeting the miR‑140‑5p/KLK10 axis". Experimental and Therapeutic Medicine 31.5 (2026): 134.
Chicago
Duan, R., Tao, Z., Tao, S., Yang, A., Yang, X., Li, C., Zhu, X., Zhang, K., Li, Z., Tao, S."Long non‑coding RNA KCNQ1OT1 promotes ovarian cancer cell malignant characteristics by targeting the miR‑140‑5p/KLK10 axis". Experimental and Therapeutic Medicine 31, no. 5 (2026): 134. https://doi.org/10.3892/etm.2026.13129
Copy and paste a formatted citation
x
Spandidos Publications style
Duan R, Tao Z, Tao S, Yang A, Yang X, Li C, Zhu X, Zhang K, Li Z, Tao S, Tao S, et al: Long non‑coding RNA KCNQ1OT1 promotes ovarian cancer cell malignant characteristics by targeting the miR‑140‑5p/KLK10 axis. Exp Ther Med 31: 134, 2026.
APA
Duan, R., Tao, Z., Tao, S., Yang, A., Yang, X., Li, C. ... Tao, S. (2026). Long non‑coding RNA KCNQ1OT1 promotes ovarian cancer cell malignant characteristics by targeting the miR‑140‑5p/KLK10 axis. Experimental and Therapeutic Medicine, 31, 134. https://doi.org/10.3892/etm.2026.13129
MLA
Duan, R., Tao, Z., Tao, S., Yang, A., Yang, X., Li, C., Zhu, X., Zhang, K., Li, Z., Tao, S."Long non‑coding RNA KCNQ1OT1 promotes ovarian cancer cell malignant characteristics by targeting the miR‑140‑5p/KLK10 axis". Experimental and Therapeutic Medicine 31.5 (2026): 134.
Chicago
Duan, R., Tao, Z., Tao, S., Yang, A., Yang, X., Li, C., Zhu, X., Zhang, K., Li, Z., Tao, S."Long non‑coding RNA KCNQ1OT1 promotes ovarian cancer cell malignant characteristics by targeting the miR‑140‑5p/KLK10 axis". Experimental and Therapeutic Medicine 31, no. 5 (2026): 134. https://doi.org/10.3892/etm.2026.13129
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