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Updated: Mar 2, 2026

MicroRNA Amplification and Recognition through Locked-nucleic-acid In situ Hybridization as a Novel Detection and Quantification Method
Published on: October 7, 2025
MicroRNA-645 is an oncogenic regulator in colon cancer
1Department of Molecular Biology, Shanxi Cancer Hospital and Institute, Shanxi, China.
Abstract:
Despite advances in early diagnosis and the development of molecularly targeted therapy, curative treatment of colon cancer once it has metastasized is yet to be accomplished. This is closely associated with deregulated CRC cell proliferation and resistance to apoptosis. Here we reveal that upregulation of microRNA-645 (miR-645) through DNA copy number gain is responsible for enhanced proliferation and resistance to apoptosis in colon cancer. MiR-645 was upregulated in most colon cancer tissues related to adjacent normal mucosa. This appeared to be associated with amplification of a section of chromosome 20q13.13, where miR-645 is located. Inhibition of miR-645 reduced proliferation and enhanced sensitivity to apoptosis triggered by the chemotherapeutic drugs 5-fluorouracil and cisplatin in CRC cells, and retarded colon cancer xenograft growth. Conversely, overexpression of miR-645 in normal colon epithelial cells enhanced proliferation and triggered anchorage-independent cell growth. Although SRY-related HMG-box 30 (SOX30) was identified as a miR-645 target, its expression was only partially affected by miR-645, suggesting that miR-645 is a fine-tuning mechanism of SOX30 expression. Moreover, overexpression of SOX30 only moderately inhibited promotion of CRC cell proliferation by miR-645, indicating that miR-645 may have more targets that contribute to its pro-proliferation effect in colon cancer. Together, this study reveals that miR-645 can regulate oncogenesis in colon cancer with SOX30 being one of its targets.
Insights
MicroRNA-645 (miR-645) upregulation drives colon cancer growth and apoptosis resistance. Inhibiting miR-645 suppressed tumor growth and increased chemotherapy sensitivity in colon cancer models.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Metastatic colon cancer remains difficult to treat, with uncontrolled cell proliferation and apoptosis resistance being key challenges.
- MicroRNAs play crucial roles in cancer development and progression.
- Understanding novel molecular drivers is essential for developing effective colon cancer therapies.
Purpose of the Study:
- To investigate the role of microRNA-645 (miR-645) in colon cancer pathogenesis.
- To determine the relationship between miR-645, cell proliferation, and apoptosis resistance.
- To identify potential therapeutic strategies targeting miR-645 in colon cancer.
Main Methods:
- Analysis of miR-645 expression in colon cancer tissues and adjacent normal mucosa.
- Investigating the association between miR-645 and chromosomal copy number alterations.
- In vitro experiments involving inhibition and overexpression of miR-645 in colon cancer cells.
- In vivo studies using colon cancer xenograft models.
- Identification and validation of miR-645 targets, including SOX30.
Main Results:
- miR-645 was significantly upregulated in colon cancer tissues, correlating with DNA copy number gain at chromosome 20q13.13.
- Inhibition of miR-645 reduced colon cancer cell proliferation, enhanced apoptosis, and suppressed tumor growth in vivo.
- Overexpression of miR-645 in normal colon cells promoted proliferation and anchorage-independent growth.
- SOX30 was identified as a miR-645 target, but miR-645's pro-proliferative effects likely involve additional targets.
Conclusions:
- Upregulation of miR-645 via DNA copy number gain is a key driver of colon cancer proliferation and apoptosis resistance.
- miR-645 represents a potential therapeutic target for colon cancer treatment.
- Further research is needed to elucidate all targets and mechanisms through which miR-645 promotes colon cancer oncogenesis.
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