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Sheykhhasan, M.;  Tanzadehpanah, H.;  Yazdi, A.A.;  Mahaki, H.;  Seyedebrahimi, R.;  Akbari, M.;  Manoochehri, H.;  Kalhor, N.;  Dama, P. FLVCR1-AS1 and FBXL19-AS1 in Multiple Human Cancers. Encyclopedia. Available online: https://encyclopedia.pub/entry/39624 (accessed on 09 July 2025).
Sheykhhasan M,  Tanzadehpanah H,  Yazdi AA,  Mahaki H,  Seyedebrahimi R,  Akbari M, et al. FLVCR1-AS1 and FBXL19-AS1 in Multiple Human Cancers. Encyclopedia. Available at: https://encyclopedia.pub/entry/39624. Accessed July 09, 2025.
Sheykhhasan, Mohsen, Hamid Tanzadehpanah, Amirhossein Ahmadieh Yazdi, Hanie Mahaki, Reihaneh Seyedebrahimi, Mohammad Akbari, Hamed Manoochehri, Naser Kalhor, Paola Dama. "FLVCR1-AS1 and FBXL19-AS1 in Multiple Human Cancers" Encyclopedia, https://encyclopedia.pub/entry/39624 (accessed July 09, 2025).
Sheykhhasan, M.,  Tanzadehpanah, H.,  Yazdi, A.A.,  Mahaki, H.,  Seyedebrahimi, R.,  Akbari, M.,  Manoochehri, H.,  Kalhor, N., & Dama, P. (2022, December 30). FLVCR1-AS1 and FBXL19-AS1 in Multiple Human Cancers. In Encyclopedia. https://encyclopedia.pub/entry/39624
Sheykhhasan, Mohsen, et al. "FLVCR1-AS1 and FBXL19-AS1 in Multiple Human Cancers." Encyclopedia. Web. 30 December, 2022.
FLVCR1-AS1 and FBXL19-AS1 in Multiple Human Cancers
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This entry is adapted from the peer-reviewed paper 10.3390/ncrna9010001

LncRNAs can operate as decoys by binding to microRNAs or transcription factors to sequester them away from their target locations and obstruct transcription and translation. The role of lncRNA as competing endogenous RNAs (ceRNAs) in the development of cancer has been demonstrated. Through their regulatory effects on DNA sequences in cis-acting and trans-acting lncRNAs, the lncRNAs can modulate many biological processes such as cell growth, proliferation, differentiation, invasion, progression, apoptosis, epithelial–mesenchymal transition (EMT), and tumorigenesis. There is growing proof that lncRNAs interact with DNA in sequence-specific ways by forming triple helix (triplex) structures. The transcriptional factors bound on a specific DNA sequence that take control of the gene expression frequently interact with LncRNA. On the other hand, LncRNA co-transcriptionally form RNA-DNA hybrids such as R-loops recognized by chromatin modifiers or by transcription factors to activate or inhibit target gene transcription.

LncRNA FLVCR1-AS1 FBXL19-AS1 cancer molecular mechanisms

1. The Effect of FLVCR1-AS1 on Several Cancers

1.1. Cholangiocarcinoma

Cholangiocarcinoma is a bile duct gastrointestinal highly heterogeneous cancer at genomic, epigenetic, and molecular levels with a limited outcome to surgical treatment, radiotherapy, and chemotherapy. To date, cholangiocarcinoma (CCA), in most cases, is diagnosed when it is advanced, often unresectable, and combined with an aggressive nature, and because of CCA, early diagnosis is difficult. It has progressed into a poor prognosis. Their incidence is globally increasing. Therefore, identifying molecular and new epigenetic biomarkers in CCA development is a crucial diagnostic tool and can help with the efficacy of the available treatments [1].
A study investigated the oncogenic effect of FLVCR1-AS1 in regulating human CCA cell proliferation, migration, and invasion. The authors first demonstrated that the expression level of FLVCR1-AS1 was significantly increased in CCA tissue compared with the adjacent normal tissues and in CCA cell lines. Bioinformatics analysis and reporter assay revealed that the lncRNA FLVCR1-AS1 acts as an oncogene sponging the miR-485-5p. As the authors pointed out, it would be interesting to investigate the broad molecular mechanism proposing it as a novel diagnostic marker for CCA [2].

1.2. Hepatocellular Carcinoma

Hepatocellular carcinoma is a relatively common type of liver tumor. Numerous lncRNAs have been described as involved in the development and progression of HCC [3][4]. A study demonstrated that FLVCR1-AS1 plays an important function in the growth and progression of HCC by sponging miR-513c [5]. The LncRNA was highly upregulated in HCC tissues and cell lines. The FLVCR1-AS1 expression level was positively correlated with tumor severity, and its knockdown remarkably inhibited HCC cell proliferation, migration, and invasion in vitro and in vivo [5].

1.3. Gastric Cancer

Although the prevalence of gastric cancer can be reduced by good nutritional habits and treatment of Helicobacter pylori, it is still one of the most common cancers with high mortality [6][7]. Several studies have reported different miRNA expression changes in gastric cells, and this aberrant expression can regulate cell proliferation and metastasis [8][9][10][11]. Moreover, ectopic expression of lncRNAs regulates the gene expression both in the nucleus and cytoplasm, leading to gastric cancer progression [11]. In the recent review, it is documented that Lnc DLX6-AS1 is as a crucial agent for the growth and proliferation of GC [12]. Liu et al. reported that an upregulated expression of FLVCR1-AS1 in gastric cancer cells by sponging miR-155 could increase the proliferation and invasion of gastric cells, implying its role in tumorigenesis [13].

1.4. Colorectal Cancer

Colorectal cancer is the second-most common cause of cancer death in men and women [14]. Diagnostic biomarkers for the early detection of CRC are still an unmet need. A pilot study pointed to the role of circulating lncRNAs as potential biomarkers. A total of 13 candidates upregulated in the plasma of 18 CRC patients were investigated. Interestingly the sensitivity in an early stage of lncRNA 91H, PVT-1, and MEG3, compared to the combination of CEA and CA19-9, currently in use for detection, was increased [15]. To shed light on the possible role of FLVCR1-AS1, in an experimental study, Han et al. compared 26 samples of CRC tissues with matched adjacent non-tumor tissues. They also measured the relative expression on CRC cell lines. lncRNA FLVCR1-AS1 resulted in upregulated in CRC cells and tissues; therefore, phenotypic assays showed a positive correlation on increasing CRC cell viability, migration, and invasion through regulation of the Mir 381/RAP2A axis. The authors suggested targeting FLVCR1-AS1 as a novel approach for treating CRC [16]. In another study, LncFLVCR1-AS1 acts as a miR-493-3p sponge to modulate cancer cell proliferation, invasion, and migration in CRC [17].

1.5. Glioma and Glioblastoma

Glioma originates from glial cells and has been identified as one of the most common fatal intracranial tumors. Despite the progress and the benefit in clinical stratification of patients due to understanding the molecular biology and genetics of GC, the impact on high mortality has not been affected. Thus, it is crucial to identify novel functional molecular targets involved in glioma development [18]. LncRNA FLVCR1-AS1 expression was upregulated in glioma tissue and cell lines and modulated E2F2 expression by sponging miR-4731-5p. The research showed the role of the FLAVR1-AS1/miR-4731-5p/E2F2 axis as a diagnostic marker of poor outcomes and as a potential target for tumor therapy [19]. Furthermore, another study has indicated that FLVCR1-AS1 is involved in the development and progression of glioma cancer. In that study, FLVCR1-AS1 expression was significantly upregulated in GBM tissues and cell lines compared with adjacent normal brain samples and human astrocyte cells, respectively. The authors, by luciferase reporter assay and rescue experiments, demonstrated that FLVCR1-AS1 acts as ceRNA for miR-30b-3p, suppressing cellular proliferation and invasion in various types of cancer, including gliomas. In addition, herein, the conclusion led to the use of FLVCR1-AS1 as a novel therapeutic target and diagnostic biomarker [20].

1.6. Non-Small Cell Lung Cancer

Lung cancer is still the leading cause of cancer death. Non-small cell lung cancer accounts for approximately 85% of all lung cancer cases. Changes in medical practice related to cancer screening and/or treatment resulted in a decline in lung cancer incidence and mortality, as reported [14]. Even though the 5-year survival rate for NSCLC is an average of 26%, compared to 7% for small cell lung cancer (cancer.net). Progress has been made to discover lncRNA biomarkers in lung cancer, such as MALAT-1, HOTAIR, and CCAT2 [21]. Gao et al., in their study, suggested FLAVCR1-AS1 as a novel diagnostic biomarker and therapeutic target [22]. The authors explored the regulatory mechanism describing the association of human NSCLC with the FLVCR1-AS1/miR-573/E2F3 axis as an important signaling pathway in tumorigenesis and progression of the disease. FLVCR1-AS1 is upregulated in the cancer tissue and cell lines, and acting as ceRNA enhances E2F3 expression through the competition of the suppressive role of miR-57 [22]. Silencing FLVCR1-AS1 repressed the proliferation, migration, and invasion of lung cancer cells, as also reported in another study where it has been revealed that FLVCR1-AS1 positively regulates the activation of the Wnt/β-catenin pathway [22][23]. The expression level of downstream targets, including proteins such as CTNNB1, SOX4, CCND1, CCND2, c-MYC, and β-catenin, was decreased. Thus, FLVCR1-AS1 could play a crucial role in the formation and development of lung cancer [23].

1.7. Ovarian Cancer

Ovarian cancer is fatal cancer in women. The prognosis of OC remains dismal as the survival rate is about 5 years in 30% of patients. An initial diagnosis of OC is required for more successful treatment [14]. A total of 85% of ovarian cases are represented by serious ovarian cancer. An investigation into the molecular mechanism suggested that the high expression of FLVCR1-AS1 induces OC by regulating the miR-513/YAP1 signaling pathway FLVCR1-AS1 expression was upregulated in OSC tissue, serums, and cell lines resulting in EMT, migration, progression, invasion, and inhibition of apoptosis [24].

1.8. Breast Cancer

Breast cancer is one of the most common malignancies in women [14]. Despite significant advances in screening and chemotherapy techniques, the survival rate is still less than 5 years after diagnosis. The incidence rate of breast cancer is rapidly growing. So, the diagnosis of the source of the disease can help in the treatment and prognosis of the disease [25][26]. The role of FLVCR1-AS1 in breast cancer has been reported by Pan et al. (2020). They showed that FLVCR1-AS1 was significantly upregulated in BC cells. The expression of FLVCR1-AS1 was found to be positively correlated with tumor growth, size, and volume in vivo, which supported that FLVCR1-AS1 played an oncogenic role in BC. Furthermore, FLVCR1-AS1 promotes proliferation and migration and activates the Wnt/β-catenin pathway through the miR-381-3p/CTNNB1 axis in breast cancer. Silencing FLVCR1-AS1 inhibited cell proliferation and inhibition of miR-381-3p, which was identified as a potential target gene of FLVCR1-AS1, reversed the tumor-restraining impacts of FLVCR1-AS1 depletion on BC progression [27].

1.9. Osteosarcoma

Osteosarcoma is the most common bone cancer in children and young people. Due to the high mortality of this cancer, specific biomarkers associated with OS tumorigenesis, progression, and distant metastasis, including from the lncRNA category, still need to be identified to help the development and implementation of more effective treatments. A great number of lncRNAs implicated in many tumorigenesis signaling pathways are dysregulated in osteosarcoma [28].
A study conducted by Jiang et al. has indicated that LncRNA FLVCR1-AS1 may promote proliferation, migration, and invasion of osteosarcoma cells by regulating the Wnt/β-catenin pathway [29].

1.10. Pancreatic Cancer

Pancreatic cancer is one of the most lethal cancer due to late diagnosis, grave prognosis, and high metastasis incidence. A 5-years survival rate is still less than 10% [14]. Moreover, the difficulty in radical surgery and the unmet need for new treatment effective against chemotherapeutic resistance require investigation of underlying mechanisms of PC tumorigenesis to uncover a new target [14]. As it is just described for numerous cancers, including lung, breast, and ovarian cancer, FLVCR1-AS1 is a tumor regulator in cell proliferation, migration, and invasion [22][23][24][30]. Lin et al. described positive feedback between FLVR1-AS1 and Kruppel-like factor 10 (KLF10), known as a tumor suppressor by regulating the transcription level of target genes through the PTEN/AKT pathway in multiple cancers, including PC [27][31][32]. They found that FLVCR1-AS1 was significantly suppressed in PC tumor tissues and was associated with poor prognosis. Furthermore, functional studies demonstrated that FLVCR1-AS1 could act as a tumor suppressor by inhibiting PC cells.
Proliferation and migration assays both in vitro and in vivo revealed that FLVCR1-AS1 was directly transcribed by KLF10 and inversely upregulated KLF10 expression by sponging miR-513c-5p and miR-514b-5p and functioning as a ceRNA for KLF10 in PC [27].

2. The Effect of FBXL19-AS1 on Several Cancers

2.1. Hepatocellular Carcinoma

An experimental study conducted by Hao et al. illustrated that the LncRNA FBXL19-AS1/miR-342-3p pathway plays a crucial function in the proliferation, migration, and invasion of Huh7 cells treated by flavonoids of Sophorae Fructus [33]. Furthermore, another study revealed a positive correlation between FBXL19-AS1 TNM stage and poor prognosis of HCC patients, where FBXL19-AS1 acts as a regulation agent, controlling HCC-associated pathways, including cell cycle, microRNAs in cancer, viral carcinogenesis via ceRNA network [29]. Consequently, this lncRNA may be considered a diagnostic and prognostic biomarker [34]. Furthermore, a study demonstrated that lncRNA FBXL19-AS1 has a diagnostic biomarker potential and is considered an appropriate candidate as a prognosis biomarker in HCC [35].

2.2. Gastric Cancer

It has been confirmed that lncRNA FBXL19-AS1 could be upregulated in gastric cancer [36][37]. Wang et al. showed that lncRNA FBXL19-AS1 could play a key role as a competing endogenous RNA to control ZEB1 expression by sponging miR-431 in gastric cancer [36]. Hence, FBXL19-AS1 may serve as a novel potential target for cancer therapy in gastric cancer. A recent study found that lncRNA FBXL19-AS1 has high expression in tumor tissues and the progress of gastric cancer via modulating miR-876-5p/HMGB4 axis [37].

2.3. Colorectal Cancer

In the study of Shen et al., 2439 lncRNAs and 1654 mRNAs were differentially expressed in metastatic CRC relative to primary CRC. Among these dysregulated lncRNAs, FBXL19-AS1 was the most significantly upregulated lncRNA in metastatic tumors. Furthermore, overexpression of FBXL19-AS1 was significantly associated with increased cell proliferation and invasion in colorectal tissue, acting as a molecular sponge in negatively modulating miR-203 [38]. Consequently, the expression of this lncRNA can be associated with colorectal cancer progression.

2.4. Glioma

Liu et al. revealed an interesting mechanism of IGF2BP2/FBXL19-AS1/ZNF765 axis on blood-tumor-barrier (BTB) permeability through tight junction-associated proteins [39]. Their study found that insulin-like grown factor 2 mRNA-binding protein 2 (RBP-IGF2BP2) and FBXL19-AS1 were overexpressed in glioma microvessel and glioma endothelial cells (GECs). In contrast, ZNF765 was lowly expressed in the comparison of ECs. When the transcription factor ZNF765 is overexpressed, it decreases the BTB permeability by inhibiting the promoter activities of tight junction-related proteins, ZO-1, occludin, and claudin-5. In this study, the authors demonstrated further the inhibition by ZNF765 on the transcriptional activity of IGF2BP2, which is shown to stabilize the expression of lnc-FBXL19-AS1 as well. In the meantime, overexpression of FBXL19-AS1 reduced the half-life of transcription factor ZNF765 mRNA via the SMD pathway and further accelerated its degradation. Consequently, FBXL19-AS1 may modulate the blood-tumor barrier permeability by negatively controlling ZNF765 via STAU1-induced mRNA decay [39].

2.5. Lung Cancer

A recent study showed that the high expression of FBXL19-AS1 drives cell proliferation and growth by regulating epithelial–mesenchymal transition (EMT) in NSCLC [40]. FBXL19-AS1 was also shown to exert a tumorigenic role in leading the progression and angiogenesis by sponging miR-431-5p to regulate RAF1 expression in lung cancer [41]. Furthermore, cell cycle analysis revealed that FBXL19-AS1 knockdown could stop the growth of tumors in the G0/G1 phase in vitro and in vivo. FBXL19-AS1/miR-203a-3p axis was found to associate with baculoviral IAP repeat-containing protein 5.1-A-like (survivin), distal-less homeobox 5, E2F transcription factor 1, and zinc finger E-box binding homeobox 2 to regulate metastasis in LUAD cells [42].

2.6. Cervical Cancer

Cervical cancer is the most preventable cancer. Unfortunately, it is persistently the second leading cause of cancer death in women aged 20 to 39. Diagnoses among young women are increasing the incidence of advanced disease and cervical adenocarcinoma, for which cytology is less effective at prevention and early detection than squamous cell carcinoma [14]. A research study investigated the role of lncRNA FBXL19-AS1 on cervical cancer proliferation, migration, invasion, apoptosis, and EMT [43]. This study demonstrated that LncRNA FBXL19-AS1 induces metastasis and proliferation of CC by acting as a ceRNA and inhibits the expression of miR-193a-5p, which negatively regulate COL1A1 expression [43]. Wan et al. indicated that FBXL19-AS1 might play an essential role in cervical cancer formation by affecting cell growth, migration, and invasion via miR-193a-5p/PIN1 signaling [44].

2.7. Breast Cancer

Recent research evaluated the functional and mechanistic roles of FBXL19-AS1 and suggested that high levels of FBXL19-AS1 expression promote migration and invasion of breast cell lines and can affect breast cancer by regulating miR-718 expression. FBXL19-AS1 might act as a diagnostic biomarker for breast cancer [45][46]. Moreover, it was demonstrated that FOXM1 upregulation inhibits tumor growth by silencing FBXL19-AS1 and that the FBXL19-AS1/miR-8765p/FOXM1 axis might regulate breast cancer cell proliferation [47]. Based on the studies’ results so far, it is possible that FBXL19-AS1 may play an important role in the tumor genesis and progression of breast cancer [46][47][48].

2.8. Osteosarcoma

A study revealed that there is an inverse relationship between FBXL19-AS1 and miR-346, where FBXL19-AS1 acts as an oncogenic marker, inducing proliferation and invasion in OS [49].

2.9. Nasopharyngeal Carcinoma

Nasopharyngeal carcinoma is a harmful and aggressive malignant tumor beginning in the nasopharyngeal epithelium [50]. Dong et al. demonstrated a relation between FBXL19-AS1 and miR-431 and PBOV1 [50]. It was identified that FBXL19-AS1 could induce the progress of nasopharyngeal carcinoma by serving as a competing endogenous RNA to sponge miR-431 and upregulate PBOV1. This study suggested that FBXL19-AS1 could be a potential therapeutic target for NPC patients. However, more studies are needed to better understand the mechanisms of action FBXL19-AS1 in NPC [50].

2.10. Acute Myeloid Leukemia

The dysregulated expression of FBXL19-AS1 has been considered related to acute myeloid leukemia. Sheng et al. demonstrated that the increased expression of FBXL19-AS1 in acute myeloid leukemia is related to clinicopathological factors, including cytogenetics (=0.021) and French-American-British classification (= 0.011) [51]. In addition, patients with upregulated FBXL19-AS1 expression had relatively short overall survival and disease-free survival. It seems that FBXL19-AS1 can be used as a potential biomarker in the diagnosis of AML [51]. However, this hypothesis needs further study and investigation in the future.

3. Molecular Mechanisms of FBXL19-AS1

Many studies have revealed that FBXL19-AS1 can regulate the expression of specific miRNAs that play an oncogenic role in various cancers. FBXL19-AS1 causes cancers by acting in different signaling pathways (Figure 1) [29][33][34][35][36][37][38][39][40][41][42][43][44][46][47][48][49][50][51].
Ncrna 09 00001 g006 550
Figure 1. Underling molecular mechanisms of FBXL19-AS1.
The EMT signaling pathway is important in cell proliferation and migration. EMT signaling pathway could be responsible for high cell proliferation and cancer development. FBXL19-AS1 can induce the EMT signaling pathway to elevate breast cancer progression through changes in the expression of EMT-related genes, such as N-cadherin and E-cadherin [48]. FBXL19-AS1 can affect cell proliferation and invasion by sponging different miRNAs [33][36][37][38][39][41][42][43][44][46][47][50]. A study demonstrated that lncRNA FBXL19-AS1 was highly expressed in breast cancer and promoted the proliferative and invasive potentials of breast cancer cells by functioning as a molecular sponge of miR-718. So, it was found that miR-718 was significantly decreased and inversely associated with FBXL19-AS1 expression in breast cancer tissues. Furthermore, they showed that FBXL19-AS1 inhibition significantly induced the expression of epithelial marker E-cadherin and decreased mesenchymal marker N-cadherin in mRNA and protein levels [46]. FBXL19-AS1 as an oncogene can also develop breast cancer through other pathways since the upregulation of FBXL19-AS1 accelerates the expression of Forkhead box M1 (FOXM1) by sponging of miR-876-5p [47]. Pan et al. (2018) suggested a critical role of FBXL19-AS1/miR-346 in osteosarcoma cell proliferation, migration, and invasion, and so inhibition of miR-346 can increase osteosarcoma [49]. Shen et al., by microarray analysis, report that 2439 lncRNAs and 1654 mRNAs were differentially expressed in metastatic CRC relative to primary CRC. Among these dysregulated lncRNAs, FBXL19-AS1 was the most significantly upregulated lncRNA in metastatic tumors [51]. Bioinformatics analysis predicted that miR-203 was potentially targeted by FBXL19-AS1, confirmed by a dual-luciferase reporter assay [42]. So, they suggested that FBXL19-AS1 may be a potential oncogenic lncRNA in CRC and FBXL19-AS1/miR-203 regulatory pathway involved in CRC tumorigenesis. Another study proved that FBXL19-AS1/miR-431-5p/RAF1 axis functions as an oncogenic pathway and plays an effective role in lung cancer. In more detail, upregulation of FBXL19-AS1 could decrease miR-431 and increase RAF1 kinase activity, which in turn increased polarity and tumor growth in colorectal cancer [42].

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Subjects: Biochemistry & Molecular Biology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Mohsen Sheykhhasan
,
Hamid Tanzadehpanah
,
Amirhossein Ahmadieh Yazdi
,
Hanie Mahaki
,
Reihaneh Seyedebrahimi
,
Mohammad Akbari
,
Hamed Manoochehri
,
Naser Kalhor
,
Paola Dama
View Times: 509
Revisions: 2 times (View History)
Update Date: 04 Jan 2023
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