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. 2024 Aug 7;23:15330338241271906. doi: 10.1177/15330338241271906

High Expression of SRSF10 Promotes Colorectal Cancer Progression by Aberrant Alternative Splicing of RFC5

Shuai Xu 1,2,#, Fangmin Zhong 1,2,#, Junyao jiang 1,2, Fangyi Yao 1,2, Meiyong Li 1,2, Mengxin Tang 2, Ying Cheng 1,2, Yulin Yang 1,2,3, Wen Wen 1,2,3, Xueru Zhang 1,2,3, Bo Huang 1,2,3,✉, Xiaozhong Wang 1,2,3,✉
PMCID: PMC11307364  PMID: 39110418

Abstract

Background

Colorectal cancer (CRC) remains a global health concern with persistently high incidence and mortality rates. However, the specific pathogenesis of CRC remains poorly understood. This study aims to investigate the role and pathogenesis of serine and arginine rich splicing factor 10 (SRSF10) in colorectal cancer.

Methods

Bioinformatics analysis was employed to predict SRSF10 gene expression in CRC patients. Functional experiments involving SRSF10 knockdown and overexpression were conducted using CCK8, transwell, scratch assay, and flow cytometry. Additionally, the PRIdictor website was utilized to predict the SRSF10 interaction site with RFC5. The identification of different transcripts of SRSF10-acting RFC5 pre-mRNA was achieved through agarose gel electrophoresis.

Result

The knockdown of SRSF10 inhibited the proliferation and migration ability of CRC cells, while promoting apoptosis and altering the DNA replication of CRC cells. Conversely, when SRSF10 was highly expressed, it enhanced the proliferation and migration ability of CRC cells and caused changes in the cell cycle of colorectal cancer cells. This study revealed a change in the replicating factor C subunit 5 (RFC5) gene in colorectal cancer cells following SRSF10 knockdown. Furthermore, it was confirmed that SRSF10 increased RFC5 exon2-AS1(S) transcription variants, thereby promoting the development of colorectal cancer through AS1 exclusion to exon 2 of RFC5.

Conclusion

In summary, this study demonstrates that SRSF10 promotes the progression of colorectal cancer by generating an aberrantly spliced exclusion isoform of AS1 within RFC5 exon 2. These findings suggest that SRSF10 could serve as a crucial target for the clinical diagnosis and treatment of CRC.

Keywords: colorectal cancer, SRSF10, alternative splicing, RFC5, splice variant

Introduction

Colorectal cancer ranks among the top three malignant tumors of the digestive system globally and is predominantly diagnosed in individuals over 40 years of age. 1 The disease's development is closely linked to long-term unhealthy lifestyle habits, an unhealthy diet, and obesity, which contribute to its slow progression and challenging early diagnosis.2,3 As a consequence, the efficacy of available treatments is often unsatisfactory, resulting in a poor prognosis.4,5 Therefore, understanding the pathogenesis of colorectal cancer is of utmost importance.

The serine/arginine-rich protein family, commonly known as SR proteins, is a group of splicing regulatory elements and serves as the primary regulators of alternative splicing by recruiting and assembling spliceosomes. 6 Among these, serine and arginine rich splicing factor 10 (SRSF10) is a prominent member of the classic SR-rich splicing factors (SRSF) and plays a crucial role in in vivo regulation of alternative splicing. On the other hand, RFC5 is a member of the replication factor C (RFC) family 7 and is an essential gene involved in base mismatch repair, cell cycle regulation, and DNA damage repair.8–10

Throughout the human body's growth and development, precursor mRNA (pre-mRNA) undergoes dynamic alternative splicing (AS). 11 Alternative splicing modifies pre-mRNA after transcription, and various splicing factors collaborate to produce mature transcriptional variants, enhancing the diversity of transcriptional variants and proteomes. Consequently, AS significantly impacts and regulates critical processes in biodiversity. 12 Pre-RNA cleavage is a tightly controlled process, involving specific identification of shearing sites, spliceosome assembly, and the influence of cis-acting elements and trans-regulators. 13 This study focuses on shear regulatory elements that are enriched in spliceosomes and exert a significant influence on alternative splicing. 6 A growing body of evidence suggests that shear regulatory elements play various roles in abnormal splicing events closely associated with CRC progression.14,15 Gaining a deeper understanding of the role of shear regulatory elements in abnormal splicing events within CRC is essential for uncovering the pathophysiological mechanisms of AS in this disease.

In this study, an analysis of the TCGA database revealed elevated expression of SRSF10 in colorectal cells compared to normal cells. Further, the knockdown of SRSF10 was found to inhibit the proliferation, invasion, and migration of colorectal cancer cells in vitro while promoting apoptosis and arresting the cell cycle at S and G2 phases. Additionally, SRSF10 knockdown affected the expression of AS1exclusion isoforms of RFC5 exon 2 in colorectal cancer. These findings suggest that SRSF10 may generate an AS1excluded isoform of RFC5 exon 2 through abnormal splicing of RFC5, specifically increasing the RFC5 exon2-AS1(S) transcription variant, thereby promoting colorectal cancer progression.

Materials and Methods

Bioinformatics Method Analysis

The expression characteristics of SRSF10 in normal human samples and colorectal cancer patients (TCGA-COAD) were analyzed using data from The Cancer Genome Atlas (TCGA)(https://portal.gdc.cancer.gov/). The interaction site of SRSF10 with RFC5 was predicted using the PRIdictor website (https://www.rna-society.org/virbase/PRIdictor.html),Please refer to the detailed instructions on the website for relevant usage.

Cell Culture

A normal colon cell epithelial cell (NCM460,Gift from Cancer Institute of Zhejiang University),HCT116 and SW480 colorectal cancer adherent cells (obtained from Typical Culture Preservation Committee Cell Bank, Chinese Academy of Sciences) were cultured in complete medium consisting of 10% fetal bovine serum(Gibco,US), 1% biclonal antibody(Servicebio,CHN) in DMEM, and L15 (Fuheng Biologics,CHN) with 10% fetal bovine serum (Gibco,US) and biclonal antibody(Servicebio,CHN). The cells were maintained at 37 °C under 5% CO2 saturation humidity.

Lentiviral Transfection and Stabilization of Cell Lines

Lentiviral transfection of adenovirus shSRSF10 was performed using a three-plasmid lentiviral system. The carrier plasmid of shSRSF10, psPAX2 vector, and pMD2G vector were co-transfected into 293 T cells using the LipofiterTM transfection reagent. The lentiviral shRNA sequence (F: 5'-GUGUACAGUUCUUCACGCU-3’, R: 5'-AGCGUAGAACUGUACACU-3’) was then transfected into SW480 and HCT116 cells at a cell density of 1 × 105 cells/well in six-well plates. After 24 h of lentiviral transfection, the medium was changed, and the cells were screened with puromycin for at least 2 weeks to establish stable cell lines.

Real-Time Quantitative Reverse Transcription Polymerase Chain Reaction (qRT–PCR)

Total RNA from the cell lines was extracted using TRIZOL reagent (Invitrogen,US), and its concentration was determined using a spectrophotometer(Agilent,US). The A260/A280 values within the range of 1.8–2.1 were considered valid. The extracted RNA was subjected to reverse transcription using a reverse transcription kit (Takara,JP) to obtain cDNA. The obtained cDNA was then amplified using PCR for the target gene. GAPDH was used as an internal reference for PCR amplification.

GAPDH forward primer: 5′-CAGCCTCAAGATCATCAGCA-3′, reverse primer: 5′-TGTGGTCATGAGTCCTTCCA-3′;

SRSF10 forward primer: 5′-ACTTGATTTCTACACTCGCCG-3′, reverse primer: 5′-CCTGGGCAAACTGTATTTCAATC-3′;

RFC5 forward primer: 5′-AGAGCACCAATATGGCTTT-3′, reverse primer: 5′-AGGATGTTGGCAATGTCTGA-3′.

Western Blot (WB)

Total proteins from SW480 and HCT116 cells were extracted using RIPA lysate (Solarbio,CHN) supplemented with protease inhibitor and phosphatase inhibitor mix (NCM Biotech,CHN). The protein concentration was determined using the BCA(Tiangen,CHN) method. Subsequently, the proteins were separated by SDS-PAGE gel electrophoresis and transferred onto a polyvinylidene fluoride (PVDF) (Millipore,US)membrane.The PVDF membrane was incubated with the corresponding primary antibody(Protenintech,CHN) for 8 h, and then the membrane was washed and incubated with secondary antibody(Cell Signaling,US) for 2 h.Finality,and the protein bands were visualized using a gel imager.

Cell Proliferation Assay (CCK8)

A Cell Counting Kit-8 (Apexbio,US) was used to assess cell proliferation. The cells were seeded in 96-well plates at a density of 5000 cells/100 μl. After cell adherence, 10 μl of CCK8 solution was added to each well, ensuring the avoidance of bubbles. The plates were then incubated for 2–2.5 h. The absorbance value of each well was measured at 450 nm using a microplate reader (Perlong,CHN) at 0 h, 24 h, 48 h, and 72 h time points.

Flow Cytometry Cycle and Apoptosis

For apoptosis analysis, approximately 5 × 106 HCT116 and SW480 cells in the logarithmic phase were collected. For apoptosis detection, at least 1 × 106 cells were collected and centrifuged. The cells were then washed with pre-chilled PBS and analyzed using the Apoptosis Assay Kit(BioLegend,US) was used for staining and analyzed by flow cytometry(Agilent,US). For cell cycle analysis, over 1 × 106 cells were collected, centrifuged, and washed with pre-chilled PBS. The cells were fixed with 70% alcohol at 4 °C. The following day, after staining with cell cycle kit(BioLegend,US), the cells were analyzed by flow cytometry.

Transwell Experiment

For cell migration, 2 × 105 cells in serum-free medium were added to the upper chamber. After incubation in the incubator for at least 24 h, the 24-well plate was taken out, the chamber was removed, and the cells were washed three times with pre-cooled PBS(Solarbio,CHN) at 4 °C. Then, the cells were fixed and stained. The number of invading cells was observed, and the average was calculated. For the cell invasion test, a glial group was added to the upper chamber, and the rest of the process was the same as the cell migration test.

Scratch Test

SW480 and HCT116 cells (5 × 105) were spread in 6-well plates until the cells reached confluence. A sterile 1 ml tip was used to create a vertical scratch to ensure no cells remained at the scratch site. After rinsing with PBS, culture medium was added. The average distance between the scratch edges at 0 h and 48 h was measured under a light microscope.

Agarose gel Electrophoresis

Total RNA extracted from the cells was subjected to reverse transcription to obtain cDNA. The resulting cDNA was then amplified using PCR. The PCR amplification product (6 × 4 μl) was mixed thoroughly with DNA loading buffer and shaken to ensure uniformity. The prepared gel was placed into an electrophoresis tank(BioRad,US) filled with electrophoresis solution. Five microliters of the sample volume was loaded into the wells of the gel, and a large and small marker were added before and after the samples. The power supply was connected, and the voltage was maintained at approximately 100 V until the blue band migrated approximately 2 cm from the starting point of the gel. Subsequently, the gel was transferred to a gel imaging system(BioRad,US) for exposure and the results were saved.

Statistical Analysis

The measurement data are presented as mean ± standard deviation (±s). The t-test was employed for two-group comparisons, while one-way ANOVA was used for comparisons between multiple groups. A bilateral P value of less than 0.05 indicates statistical significance.

Results

Based on the TCGA Database, SRSF10 Expression was Upregulated in Colorectal Cancer

The expression levels of SRSF10 were analyzed in a cohort consisting of 51 normal individuals and 647 colorectal cancer patients using data from the TCGA database. The difference analysis revealed a significant increase in the expression of SRSF10 in colorectal cancer patient samples when compared with normal samples, as depicted in Figure 1.

Figure 1.

Figure 1.

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Expression level of SRSF10 in normal humans and colorectal cancer patients in TCGA dataset. (*P < 0.05,**P < 0.01,***P < 0.001).

SRSF10 Affects the Proliferation of Colorectal Cancer Cells in Vitro

In this study, the effect of shSRSF10 transfection knockdown and plasmid transfection on the expression levels of SRSF10 in SW480 and HCT116 cells was investigated, as presented in Figure 2A and 2B. The CCK-8 assay results demonstrated that the proliferative activity of cells in the SRSF10 knockdown group was significantly reduced compared to that in the shNC group. Conversely, in the SRSF10 overexpression group, the proliferation capacity of colorectal cancer cells was significantly increased when compared with the vector group cells, as illustrated in Figure 2C and 2D.

Figure 2.

Figure 2.

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SRSF10 affects the proliferation ability of colorectal cancer cells. (A-B)qRT-PCR and WesternBlot verifies expression of SRSF10 in SW480 and HCT116 cells after silencing and overexpression. (C-D) Colorectal cancer cell proliferation assay after silencing and overexpression of SRSF10. (*P < 0.05,**P < 0.01,***P < 0.001).

SRSF10 Affects the Migration and Invasion of Colorectal Cancer Cells in Vitro

The Transwell assay results demonstrated that the inhibition of SRSF10 led to a notable decrease in the migration and invasion abilities of colorectal cancer cells. Conversely, upon overexpression of SRSF10, the migration and invasion capabilities of colorectal cancer cells were significantly enhanced, as depicted in Figure 3A and 3B. The cell scratch experiment results indicated that the wounds in the sh-SRSF10 group healed at a slower rate compared to the wounds in the shNC group under the same time conditions. In contrast, in the SRSF10 overexpression group, the wounds of colorectal cancer cells healed faster than those in the vector group, as shown in Figure 3C.

Figure 3.

Figure 3.

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Alteration of SRSF10 level affected the migration and invasion of colorectal cancer cells. (A, C) Altered SRSF10 expression levels affected the migration of colorectal cancer cells. (B) Altered levels of SRSF10 affect invasion of colorectal cells. And the scale bar in the figures (A,B,C) is observed at 400 times(40 × 10).(*P < 0.05,**P < 0.01,***P < 0.001).

SRSF10 Affects Apoptosis and Cycle of Colorectal Cells in Vitro

Flow cytometry was utilized to assess apoptosis and the cell cycle in colorectal cancer cells. The results revealed a significant increase in the percentage of apoptotic cells in the SRSF10 knockdown group compared to the shNC group. Conversely, in the SRSF10 overexpression group, the percentage of apoptotic cells was significantly lower compared to the vector group, as depicted in Figure 4A. Regarding the cell cycle analysis, in the SRSF10 knockdown group, cells showed an arrest in the S and G2 phases, indicating inhibited DNA replication compared to the shNC group. In contrast, in the SRSF10 overexpression group, the cell cycle shifted from the S phase to the G2 phase, relative to the vector group cells, as shown in Figure 4B.

Figure 4.

Figure 4.

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Effects of SRSF10 on apoptosis and cycle of colorectal cancer cells. (A) Apoptosis of HCT116 and SW480 cells after knocking down and overexpressing SRSF10. (B) After cell cycle experiments. (*P < 0.05,**P < 0.01,***P < 0.001).

SRSF10 Interacts with RFC5 in Colorectal Cancer Cells

Subsequently, the study investigated the changes in downstream genes in SW480 and HCT116 cells following the knockdown of SRSF10 gene expression. The results revealed a significant downregulation of RFC5 gene expression in both SW480 and HCT116 cells transfected with shSRSF10 compared to the shNC group, as depicted in Figure 5A. RFC5 belongs to the replication factor C (RFC) family, which plays a crucial role in DNA double helix damage repair, DNA excision, and cell cycle regulation. 7 High expression of RFC5 has been reported in various cancers, including cervical cancer, lung cancer, prostate cancer, leukemia, and lymphoma.16–19 These findings suggest that RFC5 may influence cancer progression through its biological properties, although its specific splicing patterns have not been extensively explored. Since SRSF10 acts as a transcription factor, it can facilitate the production of multiple splicing variants from a single mRNA through alternative splicing. In this study, the expression of the RFC5 gene decreased in colorectal cancer cells with reduced SRSF10 levels due to shSRSF10 transfection. This suggests a mutual binding between RFC5 and SRSF10, with SRSF10 acting as the RNA-binding protein (RBP) for RFC5. The binding site between SRSF10 and RFC5 was further investigated using a protein-RNA interaction predictor (PRIdictor, http://rnainter.org/PRIdictor/). It was found that RFC5 mRNA can bind to the aspartate residue at the 212th amino acid (aa) position of SRSF10, as shown in Figure 5B and 5C.

Figure 5.

Figure 5.

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SRSF10 interacts with RFC5. (A) qRT-PCR results observed that knockdown SRSF10 affects RFC5 gene expression. (B) Prediction of sites of action of SRSF10 and RFC5 by protein-RNA interaction predictors. (*P < 0.05,**P < 0.01,***P < 0.001).

Overexpression of RFC5 Promotes the Growth and Metastasis of Colorectal Cancer with Silencing SRSF10

Given that SRSF10 is associated with the progression of colorectal cancer and promotes RFC5 gene expression. We up-regulated the expression of RFC5 in SRSF10 knockdown colorectal cancer cells, and verified the expression of RFC5 in HCT116 and SW480 cell lines by qRT-PCR, as shown in Figure 6A. Then, the results of CCK-8 assay showed that overexpression of RFC5 in sh-SRSF10 colorectal cancer cells could restore the proliferation ability of colorectal cancer, as shown in Figure 6B.Then we performed rescue experiments in Transwell and wound healing assays, as shown in Figure 6C and 6D, and found that overexpression of RFC5 could offset the effect of SRSF10 knockdown on the biological effects of colorectal cancer cells. Finally, it was shown that overexpression of RFC5 could enhance the growth and metastasis of SRSF10 knockdown colorectal cells.

Figure 6.

Figure 6.

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RFC5 rescues the biological effects of shSRSF10 colorectal cancer cells.(A)qRT-PCR results observed that expression of SRSF10 in NCM460,SW480 and HCT116 cells.(B)CCK-8 assays were conducted after 24 h, 48 h, and 72 h to test cell viability.(C)The migration and invasion abilities were determined by transwell assay.(D)Cell healing assay was used to detect cell migration ability.And the scale bar in the figures (A,B,C) is observed at 400 times(40 × 10).(*P < 0.05,**P < 0.01,***P < 0.001).

SRSF10 Affects the Alternative Splicing of RFC5 to Facilitate the Exclusion of AS1 of RFC5 exon2

In this study, we initially predicted differential gene expression following the downregulation of SRSF10. Subsequently, we identified that SRSF10 can target the site of RFC5 (12:118455800-1184558588) on exon 2,in supplementary table 1, and elucidated the underlying mechanism by comparing alternative splicing (AS) events before and after knocking down SRSF10 in cells, as illustrated in Figure 7A. Further investigations revealed that when SRSF10 was downregulated, the gene expression of RFC5 was altered. Previous studies have highlighted RFC5's role in cellular DNA damage repair and cell cycle regulation. 20 Next, in this study, specific primers for the splicing isoforms of RFC5 (RFC5 exon2(L) and RFC5 exon2-AS1(S)) were designed. cDNA was synthesized via reverse transcription, and the resulting products were subjected to detection using agarose gel electrophoresis. It was observed that compared with a normal colon cell epithelial cell (NCM460), the expression of RFC5 exon2-AS1 (S) in SW480 and HCT116 cells increased significantly, while the expression of RFC5 exon2 (L) did not change significantly, as shown in Figure 7B. Then, we found that the downregulation of SRSF10 in SW480 and HCT116 cells led to reduced AS1 skipping of RFC5 exon2, indicating a decreased expression of RFC5 exon2-AS1(S) variants, as depicted in Figure 7C.

Figure 7.

Figure 7.

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SRSF10 interacts with RFC5. (A) SRSF10 cuts the mode of RFC5 as well as yields two different transcripts. (B)The expression of RFC5 exon2-AS1 (S) and RFC5 exon2 (L) between colorectal cancer cell and a normal colon epithelial cell.(C) Detection of sh-SRSF10 affecting variable splicing of RFC5.

Discussion

In recent decades, colorectal cancer has continued to have a high incidence and mortality rate, prompting extensive research into its pathogenesis. Post-transcriptional modifications of mRNA, including alternative splicing, are common occurrences in colorectal cancer. 21 Alternative splicing has been observed in various cancers.22–25

SRSF10, a member of the SR protein family, is enriched in serine/arginine-rich proteins and plays a pivotal role in regulating alternative splicing in vivo. 26 It accomplishes this by recruiting small ribonucleoprotein (snRNP) and its cofactors to participate in the regulation of variable splicing of precursor mRNA (pre-mRNA), leading to the generation of various splicing isoforms.27,28 In this study, bioinformatics analysis of the TCGA database revealed high expression of the SRSF10 gene in colorectal cancer. Subsequently, the expression of the SRSF10 gene was altered in SW480 and HCT116 colorectal cancer cells, and experiments demonstrated that SRSF10 knockdown inhibited cell proliferation, invasion, and migration, while promoting apoptosis and causing cell cycle arrest in the S and G2 phases. Conversely, SRSF10 overexpression accelerated cell proliferation, invasion, and migration, inhibited apoptosis, reduced cell cycle arrest in the S phase, increased transition to the G2 phase, and promoted cell proliferation. These findings indicate a significant correlation between SRSF10 and the progression of colorectal cancer.

Furthermore, this study identified a significant decrease in the expression of the RFC5 gene, a member of the replication factor C (RFC) family and the fifth subunit of RFCs, in colorectal cancer cells with knocked-down SRSF10. RFC5 is primarily involved in DNA damage repair and cell cycle regulation. 16 RFC5 has also been reported as an oncogene and associated with colorectal cancer. 29 Further investigation revealed that SRSF10 may induce alternative splicing of exon 2 of RFC5. Therefore, agarose gel electrophoresis was performed using designed primers for the splicing isoform of RFC5. The experiments demonstrated a significant reduction in the expression of RFC5 exon2-AS1 (S) in colorectal cancer cells was significantly increased compared to a normal colon cell epithelial cell (NCM460). There was no significant change in the expression of RFC5 exon2 (L). Next found the splicing isoform (RFC5 exon2-AS1(S)) that underwent exon 2 exclusion in the SRSF10 knockdown colorectal cancer cells, while the expression of the splicing isoform (RFC5 exon2(L)) containing exon 2 of RFC5 was not significantly different. This suggests that SRSF10 influences the development of colon cancer by abnormally splicing RFC5 to produce the RFC5 exon2-AS1(S) isoform.

Finally, this study demonstrates that SRSF10 is highly expressed in colorectal cancer and exerts significant effects on various cellular processes, including proliferation, invasion, migration, apoptosis, and cell cycle regulation, through knockdown and overexpression experiments. The protein-RNA interaction predictor further confirms the interaction between SRSF10 and the RFC5 gene, establishing that RFC5 exon2-AS1 (S) is highly expressed in colorectal cancer cells.en attendant, knocking down SRSF10 expression can influence the expression of RFC5 exon2-AS1(S) isoform, thus impacting the progression of colorectal cancer cells. These findings establish a close association between SRSF10 and the development of colorectal cancer, highlighting its potential as a promising therapeutic target and diagnostic marker for CRC. However, this study also has some limitations. First, there is no direct experiment to prove the binding of SRSF10 to RFC5, but indirectly to prove its interaction. Second, the specific function of RFC5 exon2-AS1 (S) in colorectal cancer cells has not been studied in depth. Third, the effect of overexpression of SRSF10 on RFC5 splicing variants was not studied in colorectal cells. Future studies will also further explore the effect of RFC5 splicing variants on colorectal cells and the more detailed mechanism of SRSF10 on RFC5 alternative splicing.

Conclusion

In conclusion, this study investigates the role of SRSF10 gene expression in colorectal cancer cells. The protein-RNA interaction predictor confirms the interaction between SRSF10 and RFC5, and further experimentation demonstrates that SRSF10 promotes the AS1 exclusion of RFC5 exon 2, leading to an increased production of RFC5 exon2-AS1(S) isoform, which affects the occurrence and progression of colorectal cancer. These findings provide a basis for further research in this area.

Supplemental Material

sj-docx-1-tct-10.1177_15330338241271906 - Supplemental material for High Expression of SRSF10 Promotes Colorectal Cancer Progression by Aberrant Alternative Splicing of RFC5
sj-docx-1-tct-10.1177_15330338241271906.docx (29.9KB, docx)

Supplemental material, sj-docx-1-tct-10.1177_15330338241271906 for High Expression of SRSF10 Promotes Colorectal Cancer Progression by Aberrant Alternative Splicing of RFC5 by Shuai Xu, Fangmin Zhong, Junyao jiang, Fangyi Yao, Meiyong Li, Mengxin Tang, Ying Cheng, Yulin Yang, Wen Wen, Xueru Zhang, Bo Huang and Xiaozhong Wang in Technology in Cancer Research & Treatment

Acknowledgements

Not pplicable.

Footnotes

Authors’ Contributions: Yulin Yang, Ying Cheng carried out the conception and design of the research, Xueru Zhang,Mengxin Tang and Wen Wen participated in the acquisition of data. Fangmin Zhong, Junyao jiang carried out the analysis and interpretation of data. Fangyi Yao, Meiyong Li performed the statistical analysis. Shuai Xu, Fangmin Zhong drafted the manuscript and Bo Huang, Xiaozhong Wang and Shuai Xu participated in revision of manuscript for important intellectual content. All authors read and approved the final manuscript.

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Ethics Approval and Consent to Participate: Not applicable.

Funding: The authors received no financial support for the research, authorship, and/or publication of this article.

Supplemental Material: Supplemental material for this article is available online.

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Supplementary Materials

sj-docx-1-tct-10.1177_15330338241271906 - Supplemental material for High Expression of SRSF10 Promotes Colorectal Cancer Progression by Aberrant Alternative Splicing of RFC5
sj-docx-1-tct-10.1177_15330338241271906.docx (29.9KB, docx)

Supplemental material, sj-docx-1-tct-10.1177_15330338241271906 for High Expression of SRSF10 Promotes Colorectal Cancer Progression by Aberrant Alternative Splicing of RFC5 by Shuai Xu, Fangmin Zhong, Junyao jiang, Fangyi Yao, Meiyong Li, Mengxin Tang, Ying Cheng, Yulin Yang, Wen Wen, Xueru Zhang, Bo Huang and Xiaozhong Wang in Technology in Cancer Research & Treatment

Articles from Technology in Cancer Research & Treatment are provided here courtesy of SAGE Publications

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