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Tumor Discovery PTMAP5–hsa-miR-22-3p–KIF2C axis in HCC development

plays a pivotal role in microtubule depolymerization, growth, migration, invasion, and tumor formation in CRC
binding between microfilaments and centromeres, cells. The significant correlation between HJURP and CRC
and chromosome segregation – functions critical for suggests that it could serve as a promising biomarker for
the regulation of mitosis. Thus, the mitosis process diagnosis and prognosis, as well as a potential target for
is regulated. Research further indicates that KIF2C new drug development. Sun et al. reported that KIF4A
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is overexpressed in non-small-cell lung cancer, regulates the biological functions of esophageal squamous
breast cancer, pancreatic ductal adenocarcinoma, cell carcinoma cells and promotes their proliferation and
and other tumor types, where its elevated expression migration by affecting the phosphorylation of proteins
correlates with poor patient outcomes. 22-24 In addition, related to the Hippo signaling pathway. Wang et al.
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Li et al. identified eight kinesin superfamily reported that MCM5 correlates with alignment status
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proteins significantly correlated with tumor stage and unfavorable outcomes in cervical adenocarcinoma
and pathological grade in HCC patients, where their patients, influencing the growth of this cancer. Gong et al.
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increased expression levels were linked to poorer demonstrated that NCAPG acts as an oncogene in HCC
overall and disease-free survival rates. by promoting cell proliferation and inhibiting apoptosis
In the context of bladder cancer, KIF20A has been through activation of the PI3K/AKT/FOXO4 pathway.
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identified as a significant prognostic factor due to its role Meng et al. reported that estrogen-regulated PTTG1
in promoting the proliferation and metastasis of bladder controls the cell cycle, contributing to the development of
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cancer cells. Keyhanian et al. demonstrated that the breast cancer.
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combination of MCM2 expression with Ki67 and P16 Liu et al. revealed the emerging roles and interplay of
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immunohistochemistry can distinguish leiomyosarcoma MDM4 and TOP2A in tumor development, implying that
of the uterus. Liu et al. analyzed the mRNA and protein blocking the interaction between these proteins could be an
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levels of MCMs in tissue samples from patients with HCC, innovative approach to concurrently target both in cancer
recognizing MCM6 as a catalyst for the progression of the therapies. Agarwal et al. ’s findings suggest that TRIP13
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S/G2 cell cycle and a promising indicator for diagnosing promotes tumor growth and metastasis, regardless of p53
and predicting HCC prognosis. or microsatellite instability status, positioning it as a target
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Blackledge et al. demonstrated that PRC1 catalysis for CRC therapy. Yin et al. demonstrated that UBE2T
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is central to the function and genetic regulation of enhances cell growth, movement, migration, invasion, and
the polycomb system. Del Re et al. documented that resistance to radiation in both living organisms (in vivo)
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heightened expression of TK1 and CDK9 in exosomes and controlled environments (in vitro) by accelerating the
derived from plasma of metastatic breast cancer patients G2/M phase transition and inhibiting apoptosis.
correlated with clinical resistance to CDK4/6 inhibitors. Based on our current expression and survival analysis,
Zhou et al. showed that TPX2 promotes the metastasis these studies indicate that the 24 genes mentioned above
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and malignant progression of non-small-cell lung cancer, could potentially play crucial roles as oncogenes in the
positioning it as a marker of poor prognosis. Li et al. advancement of HCC.
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showed that TROAP plays a crucial role in fostering the
growth, infiltration, and spread of breast cancer. MiRNAs are ncRNA molecules that can inhibit the
expression of target genes and thus play an important
In a study of gastrointestinal cancer cell lines with role in regulating biological behaviour. 44,45 Therefore, we
activated KRAS, Wang-Bishop et al. reported that AURKA investigated 24 miRNAs that target genes involved in
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phosphorylates RPS6KB1, promoting cell proliferation and HCC. Using several online databases, we predicted several
tumor survival in xenograft models. Inhibiting AURKA potential miRNAs that could inhibit the occurrence and
may, therefore, slow the growth of gastrointestinal tumors development of HCC. After performing survival analysis,
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by targeting KRAS activation. Wang et al. also briefly we identified 118 miRNA‒mRNA pairs with the greatest
described the upstream regulators of CDC20 and its potential functional roles in HCC, which were then
carcinogenic role in various human malignancies. subjected to further correlation analysis. This analysis
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Sun et al. predicted that CENPF could activate the revealed that the hsa-miR-22-3P–KIF2C pair exhibited the
PI3K-Akt-mTORC1 signaling pathway to promote bone most significant negative correlation. Therefore, the hsa-
metastasis in breast cancer, identifying it as a novel target miR-22-3P–KIF2C axis is considered a potential pathway
for breast cancer treatment. Kang ’s results demonstrated involved in HCC progression. Next, we identified genes
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that deletion of the HJURP gene inhibits proliferation, co-expressed with KIF2C using the UALCAN and GEPIA
migration, invasion, and tumorigenicity in colorectal databases. UALCAN serves as a highly efficient web-based
cancer cells (CRC). The gene deletion was shown to suppress analysis tool that extracts valuable insights from cancer

Volume 3 Issue 3 (2024) 19 doi: 10.36922/td.2846