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Bioengineered Volume 13, 2022 - Issue 4
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Research Paper

Melatonin promotes apoptosis of thyroid cancer cells via regulating the signaling of microRNA-21 (miR-21) and microRNA-30e (miR-30e)

Hao JiaThyroid & Vascular Surgery Department, Zhumadian Central Hospital, Zhumadian, Henan Province, ChinaCorrespondence[email protected]
ORCID Iconhttps://orcid.org/0000-0001-6021-2644View further author information
ORCID Icon,
Wei SunThyroid & Vascular Surgery Department, Zhumadian Central Hospital, Zhumadian, Henan Province, ChinaView further author information
,
Xiangbo LiThyroid & Vascular Surgery Department, Zhumadian Central Hospital, Zhumadian, Henan Province, ChinaView further author information
&
Wenhao XuThyroid & Vascular Surgery Department, Zhumadian Central Hospital, Zhumadian, Henan Province, ChinaView further author information
Pages 9588-9601 | Received 07 Jan 2022, Accepted 11 Mar 2022, Published online: 12 Apr 2022

Figures & data

Figure 7. Luciferase assays showed that miR-21 and miR-30e suppressed the expression of PTEN and miR-21 while inhibiting the expression of lncRNA-CASC7 (* P value < 0.05, vs. control group).

A: Sequence analysis indicated potential binding of miR-21 to lncRNA-CASC7.B: The luciferase activity of wild-type lncRNA-CASC7 was inhibited by miR-21 in TPC-1 cells.C: The luciferase activity of wild-type lncRNA-CASC7 was inhibited by miR-21 in BCPaP cells.D: Sequence analysis indicated potential binding of miR-21 to PTEN.E: The luciferase activity of wild type PTEN was inhibited by miR-21 in TPC-1 cells.F: The luciferase activity of wild type PTEN was inhibited by miR-21 in BCPaP cells.G: Sequence analysis indicated potential binding of miR-30e to PTEN.H: The luciferase activity of wild type PTEN was inhibited by miR-30e in TPC-1 cells.I: The luciferase activity of wild type PTEN was inhibited by miR-30e in BCPaP cells.
Figure 7. Luciferase assays showed that miR-21 and miR-30e suppressed the expression of PTEN and miR-21 while inhibiting the expression of lncRNA-CASC7 (* P value < 0.05, vs. control group).

Figure 1. MEL treatment suppressed tumor cell growth in nude mice.

A: The tumor size of TPC-1 cells implanted in nude mice was decreased by MEL treatment.B: The weight of tumor tissues in nude mice was decreased by MEL treatment.C: The tumor size in nude mice implanted with BCPaP cells was decreased by MEL treatment.D: The weight of tumor tissues in nude mice implanted with BCPaP cells was decreased by MEL treatment.
Figure 1. MEL treatment suppressed tumor cell growth in nude mice.

Figure 2. IHC analysis showed that the expression of PTEN protein in tumor tissues in nude mice was activated by MEL treatment (* P value < 0.05, vs. control group).

A: The expression of PTEN protein in tumor tissues in nude mice implanted with TPC-1 cells was increased by MEL treatment.A: The expression of PTEN protein in tumor tissues in nude mice implanted with BCPaP cells was increased by MEL treatment.
Figure 2. IHC analysis showed that the expression of PTEN protein in tumor tissues in nude mice was activated by MEL treatment (* P value < 0.05, vs. control group).

Figure 3. MEL treatment suppressed the expression of miR-30e and miR-21 while enhancing the lncRNA-CASC7 and PTEN mRNA expression as well as H2S production in the tumor tissues of nude mice (* P value < 0.05, vs. control group).

A: The expression of miR-30e in tumor tissues in nude mice implanted with TPC-1 cells was suppressed by MEL treatment.B: The production of H2S in tumor tissues in nude mice implanted with TPC-1 cells was enhanced by MEL treatment.C: The expression of lncRNA-CASC7 in tumor tissues in nude mice implanted with TPC-1 cells in nude mice was activated by MEL treatment.D: The expression of miR-21 in tumor tissues in nude mice implanted with TPC-1 cells was repressed by MEL treatment.E: The expression of PTEN mRNA in tumor tissues in nude mice implanted with TPC-1 cells was promoted by MEL treatment.F: The expression of miR-30e in tumor tissues in nude mice implanted with BCPaP cells was suppressed by MEL treatment.G: The production of H2S in tumor tissues in nude mice implanted with BCPaP cells was enhanced by MEL treatment.H: The expression of lncRNA-CASC7 in tumor tissues in nude mice implanted with BCPaP cells was activated by MEL treatment.I: The expression of miR-21 in tumor tissues in nude mice implanted with BCPaP cells was repressed by MEL treatment.J: The expression of PTEN mRNA in tumor tissues in nude mice implanted with BCPaP cells was promoted by MEL treatment.
Figure 3. MEL treatment suppressed the expression of miR-30e and miR-21 while enhancing the lncRNA-CASC7 and PTEN mRNA expression as well as H2S production in the tumor tissues of nude mice (* P value < 0.05, vs. control group).

Figure 4. MEL inhibited the proliferation and activated the apoptosis of TPC-1 and BCPaP cells (* P value < 0.05, vs. untreated cells).

A: The proliferation of TPC-1 cells was inhibited by MEL treatment.B: The apoptosis of TPC-1 cells was activated by MEL treatment.C: The proliferation of BCPaP cells was inhibited by MEL treatment.D: The apoptosis of BCPaP cells was activated by MEL treatment.
Figure 4. MEL inhibited the proliferation and activated the apoptosis of TPC-1 and BCPaP cells (* P value < 0.05, vs. untreated cells).

Figure 5. The expression of PTEN protein in TPC-1 and BCPaP cells was enhanced by MEL treatment (* P value < 0.05, vs. untreated cells).

A: The expression of PTEN protein in TPC-1 cells was activated by MEL treatment.B: The expression of PTEN protein in BCPaP cells was activated by MEL treatment.
Figure 5. The expression of PTEN protein in TPC-1 and BCPaP cells was enhanced by MEL treatment (* P value < 0.05, vs. untreated cells).

Figure 6. MEL treatment suppressed the expression of miR-30e and miR-21 while enhancing the lncRNA-CASC7 and PTEN mRNA expression as well as H2S production in TPC-1 and BCPaP cells (* P value < 0.05, vs. untreated cells).

A: The expression of miR-30e in TPC-1 cells was suppressed by MEL treatment.B: The production of H2S in TPC-1 cells was enhanced by MEL treatment.C: The expression of lncRNA-CASC7 in TPC-1 cells was activated by MEL treatment.D: The expression of miR-21 in TPC-1 cells was repressed by MEL treatment.E: The expression of PTEN mRNA in TPC-1 cells was promoted by MEL treatment.F: The expression of miR-30e in TPC-1 cells was suppressed by MEL treatment.G: The production of H2S in TPC-1 cells was enhanced by MEL treatment.H: The expression of lncRNA-CASC7 in TPC-1 cells was activated by MEL treatment.I: The expression of miR-21 in TPC-1 cells was repressed by MEL treatment.J: The expression of PTEN mRNA in TPC-1 cells was promoted by MEL treatment.
Figure 6. MEL treatment suppressed the expression of miR-30e and miR-21 while enhancing the lncRNA-CASC7 and PTEN mRNA expression as well as H2S production in TPC-1 and BCPaP cells (* P value < 0.05, vs. untreated cells).
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Melatonin promotes apoptosis of thyroid cancer cells via regulating the signaling of microRNA-21 (miR-21) and microRNA-30e (miR-30e)
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