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Apolipoprotein m promotes growth and inhibits apoptosis of colorectal cancer cells through upregulation of ribosomal protein s27a

Mu, Qinfeng (author)
Third Affiliated Hospital of Soochow University
Luo, Guanghua (author)
Third Affiliated Hospital of Soochow University
Wei, Jiang (author)
Third Affiliated Hospital of Soochow University
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Zheng, Lu (author)
Third Affiliated Hospital of Soochow University
Wang, Haitao (author)
Third Affiliated Hospital of Soochow University
Yu, Miaomei (author)
Third Affiliated Hospital of Soochow University
Xu, Ning (author)
Lund University,Lunds universitet,Avdelningen för klinisk kemi och farmakologi,Institutionen för laboratoriemedicin,Medicinska fakulteten,Division of Clinical Chemistry and Pharmacology,Department of Laboratory Medicine,Faculty of Medicine
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 (creator_code:org_t)
2021
2021
English 15 s.
In: EXCLI Journal. - 1611-2156. ; 20, s. 145-159
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Colorectal cancer (CRC) is one of the frequent malignant tumors and has a high mortality-to-incidence ratio. Apolipoprotein M (ApoM), a lipoprotein superfamily member, is primarily bound to high-density lipoprotein (HDL) particles. Our previous studies opined that ApoM crucially modulates CRC progression, but its role in CRC has not been elucidated. Here, lentivirus infection technology was used to overexpress ApoM in Caco-2 cells. Cell growth, apoptosis as well as clone formation assays were performed to explore the biological influences of ApoM in Caco-2 cells. Differentially expressed genes were analyzed via GeneChip microarrays and Quantitative real-time PCR (qPCR) along with Western blotting were applied to verify the results. Ribosomal protein S27a (RPS27A) expression in CRC and tumor-adjacent tissues was detected by qPCR, and its correlation with clinico-pathologic characteristics was explored. Our results showed that ApoM overexpression could promote Caco-2 cell proliferation and inhibit apoptosis. The microarray evaluation uncovered 2671 genes, which were differentially expressed, including RPS27A. The qPCR as well as the Western blotting data showed that ApoM overexpression significantly increased the expression of RPS27A. Moreover, RPS27A expression was remarkably higher in CRC tissues in contrast with the tumor-adjacent tissues and was positively correlated with the ApoM level in tumor tissues, and higher RPS27A expression was associated with smaller tumors and lower T stage. Functional recovery experiments indicated that knockdown of RPS27A counteracted the apoptosis inhibition and clone formation pro-motion induced by ApoM overexpression in Caco-2 cells. In conclusion, ApoM promotes CRC cell growth and inhibits apoptosis through upregulation of RPS27A.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Cancer och onkologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Cancer and Oncology (hsv//eng)

Keyword

Apolipoprotein M
Apoptosis
Colorectal cancer
GeneChip microarrays
Growth
Ribosomal protein S27a

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By the author/editor
Mu, Qinfeng
Luo, Guanghua
Wei, Jiang
Zheng, Lu
Wang, Haitao
Yu, Miaomei
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Xu, Ning
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About the subject
MEDICAL AND HEALTH SCIENCES
MEDICAL AND HEAL ...
and Clinical Medicin ...
and Cancer and Oncol ...
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EXCLI Journal
By the university
Lund University

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